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Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management
Open accessAbstract
An impaired glucose metabolism, which often leads to the onset of diabetes mellitus (DM), is a common complication of chronic exposure to exogenous and endogenous glucocorticoid (GC) excess and plays an important part in contributing to morbidity and mortality in patients with Cushing syndrome (CS). This article reviews the pathogenesis, epidemiology, diagnosis, and management of changes in glucose metabolism associated with hypercortisolism, addressing both the pathophysiological aspects and the clinical and therapeutic implications. Chronic hypercortisolism may have pleiotropic effects on all major peripheral tissues governing glucose homeostasis. Adding further complexity, both genomic and nongenomic mechanisms are directly induced by GCs in a context-specific and cell-/organ-dependent manner. In this paper, the discussion focuses on established and potential pathologic molecular mechanisms that are induced by chronically excessive circulating levels of GCs and affect glucose homeostasis in various tissues. The management of patients with CS and DM includes treating their hyperglycemia and correcting their GC excess. The effects on glycemic control of various medical therapies for CS are reviewed in this paper. The association between DM and subclinical CS and the role of screening for CS in diabetic patients are also discussed.
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TL;DR
This review synthesizes molecular, epidemiological, diagnostic, and therapeutic evidence on glucose metabolism abnormalities in endogenous and exogenous Cushing syndrome, emphasizing that hypercortisolism causes insulin resistance and impaired insulin secretion. It concludes that controlling hypercortisolism is central to glycemic improvement, but evidence for optimal antidiabetic therapy in CS remains limited.
Key findings
- In endogenous CS, 20%–45% of patients have DM and 10%–30% have defective glucose tolerance, with overall glucose metabolism impairment approaching 70%; fasting plasma glucose may be normal in 64% of endogenous CS patients with DM.
- Exogenous GC use carries dose-dependent DM risk: nearly 9% of patients with rheumatoid arthritis developed DM within 2 years of starting GC treatment; odds ratios for starting an oral hypoglycemic agent or insulin were 1.77, 3.02, 5.82, and 10.34 for hydrocortisone-equivalent doses of 1–39, 40–79, 80–119, and ≥120 mg/d, respectively; a meta-analysis reported an odds ratio of 1.5 to 2.5 for newly diagnosed DM with exogenous GCs.
- In subclinical CS/adrenal incidentalomas, DM or IGT was identified in 20%–25% of patients with AI and SCS, though prevalence varied with screening methods and diagnostic criteria.
- Medical therapy effects varied: ketoconazole improved glycemic control in 56% of diabetic patients in a series of 200 CD patients; mifepristone reduced OGTT glucose AUC by at least 25% in 60% of patients with DM/IGT (median decrease 36%); cabergoline reduced DM prevalence from 25% to 10% and IGT from 37.5% to 20% after 24 months in responsive patients; pasireotide caused hyperglycemia in up to 73% and 6% discontinued treatment because of hyperglycemia-related adverse events or uncontrolled DM.
Methods
- Design: narrative review of the pathogenesis, epidemiology, diagnosis, and management of changes in glucose metabolism associated with hypercortisolism, addressing pathophysiological and clinical/therapeutic implications.
- Data: cited literature and summary tables on prevalence of DM/glucose intolerance in CS, adrenal incidentalomas, screening for CS in type 2 DM, and medication effects; no primary patient sample or systematic search strategy is described.
- Analysis: qualitative synthesis of molecular mechanisms and clinical evidence; no meta-analysis or formal risk-of-bias assessment is described.
Limitations
- Stated: there is a lack of studies specifically investigating antidiabetic therapy in endogenous CS and few studies in exogenous GC-induced hyperglycemia; evidence on optimal antidiabetic treatment is scarce, and recommendations are based largely on current best practice.
- Stated: there is no general consensus on diagnostic criteria for SCS, and prevalence estimates vary with screening methods and criteria.
- Evident: as a narrative review, it does not report a systematic search, meta-analysis, or primary data; many cited therapeutic studies are retrospective, small, or uncontrolled.
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In the paper
“There may also be indirect effects of GCs on peripheral insulin sensitivity and glucose homeostasis through GC-dependent changes in protein and lipid metabolism, as well as GC-mediated impairments in interorgan communication conducted by organderived circulating factors.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Pathogenesis of DM in CS
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In the paper
“Chronic hypercortisolism may have pleiotropic effects on all major peripheral tissues governing glucose homeostasis.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Abstract
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In the paper
“In the liver, the aberrant HGO that contributes to hyperglycemia is attributed largely to the transcriptional upregulation of key gluconeogenic enzymes.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“In particular, GCs profoundly alter the hepatic action of insulin, resulting in exacerbated gluconeogenesis and hepatic glucose output (HGO) through both direct and indirect effects on the mechanisms controlling these processes.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“A second important effect of GCs in the liver is to induce a selective IR that impedes the inhibitory effect of insulin on HGO while preserving the lipogenic effect of the hormone.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“In the liver, chronic hypercortisolism impairs fasting and postprandial glucose and lipid metabolism.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“Interestingly, recent studies indicate that GCs may also stimulate lipogenesis in the liver through epigenetic mechanisms involving microRNAs.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“GCs bind and activate a superfamily of nuclear receptors [glucocorticoid receptors (GCRs)] that control the transcription of certain genes in a cell-and tissue-specific manner by binding directly to genomic glucocorticoid response elements (GCREs) or by tethering to other DNA-binding transcription factors.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“Impaired glucose metabolism may be an important contributor to the higher cardiovascular morbidity and mortality in patients with CS.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Abstract
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In the paper
“Higher plasma mineralocorticoid levels may be associated with IR (, ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
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In the paper
“In conclusion, the lack of studies on the effects of different antidiabetic agents in CS patients with altered glucose homeostasis has complicated development of guidelines on an optimal antidiabetic strategy for such patients.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Conclusions
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An impaired glucose metabolism, which often leads to the onset of diabetes mellitus (DM), is a common complication of chronic exposure to exogenous and endogenous glucocorticoid (GC) excess and plays an important part in contributing to morbidity and mortality in patients with Cushing syndrome (CS).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Abstract
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Surprisingly, only % of patients with CS developed hepatic steatosis (, ), suggesting that lipotoxicity associated with aberrant lipid storage in hepatocytes is not a predominant pathologic mechanism of IR in this disease.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced hepatic metabolic disorders
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In the paper
“GC excess may impair glucose metabolism through many complex pathophysiological mechanisms and is associated with varying degrees of glucose intolerance, including impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and overt diabetes mellitus (DM).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Abstract
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In the paper
“Adding further complexity, both genomic and nongenomic mechanisms are directly induced by GCs in a contextspecific and cell-/organ-dependent manner.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Abstract
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In the paper
“Abdominal obesity is closely associated with metabolic syndrome and CS.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Consequences of hypercortisolism on adipose tissue
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In the paper
“The precise mechanisms underlying these pathologic GC-induced outcomes in muscle are still not entirely clear, but they too appear to stem from pleiotropic effects that contribute to impairment of insulin signaling and glucose uptake.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC-induced alterations of glucose metabolism in skeletal muscles
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In the paper
“Several other mechanisms of aldosterone-induced glucose intolerance have been suggested, including effects on insulin signaling, stimulation of hepatic gluconeogenesis, effects on sodium-glucose transport, and fibrosis-induced dysfunction in insulin-producing or insulin-sensitive tissues.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
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In the paper
“It has been suggested that nongenomic actions of MRs might result in increased collagen synthesis and fibrosis, not only in the heart but also in other insulin-sensitive tissues such as the pancreas, liver, fat, and”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
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In the paper
“Similarly, patients with PA had low adiponectin levels with an associated weaker insulin sensitivity ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
- Not checked yetcites [178] Cooper, 2007, Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance, Am J Physiol Heart Circ Physiol source
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None of the sources cited for this claim have been checked yet.
In the paper
“From % to % of patients with endogenous CS have DM, and % to % have defective glucose tolerance, so the overall prevalence of glucose metabolism impairments can come close to %, as shown in Table (, , -).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Endogenous CS
What the sources say
- Not checked yetcites [107] Giordano, 2014, Is diabetes in Cushing’s syndrome only a consequence of hypercortisolism?, Eur J Endocrinol source
- Not checked yetcites [143] Ferron, 2014, Regulation of energy metabolism by the skeleton: osteocalcin and beyond, Arch Biochem Biophys source
- Not checked yetcites [181] Friedman, 1996, Carbohydrate and lipid metabolism in endogenous hypercortisolism: shared features with metabolic syndrome X and NIDDM, Endocr J source
- Not checked yetcites [182] Biering, 2000, Prevalence of diabetes in acromegaly and Cushing syndrome [in German], Acta Med Austriaca source
- Not checked yetcites [183] Faggiano, 2003, Cardiovascular risk factors and common carotid artery caliber and stiffness in patients with Cushing’s disease during active disease and 1 year after disease remission, J Clin Endocrinol Metab source
- Not checked yetcites [184] Pecori Giraldi, 2003, Study Group on the Hypothalamo-Pituitary-Adrenal Axis of the Italian Society of Endocrinology. Gender-related differences in the presentation and course of Cushing’s disease, J Clin Endocrinol Metab source
- Not checked yetcites [185] Mancini, 2004, High cardiovascular risk in patients with Cushing’s syndrome according to 1999 WHO/ISH guidelines, Clin Endocrinol (Oxf) source
- Not checked yetcites [186] Giordano, 2011, Metabolic and cardiovascular outcomes in patients with Cushing’s syndrome of different aetiologies during active disease and 1 year after remission, Clin Endocrinol (Oxf) source
- Not checked yetcites [187] Valassi, 2011, The European Registry on Cushing’s syndrome: 2-year experience. Baseline demographic and clinical characteristics, Eur J Endocrinol source
- Not checked yetcites [188] Dekkers, 2013, Multisystem morbidity and mortality in Cushing’s syndrome: a cohort study, J Clin Endocrinol Metab source
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In the paper
“MRs on adipocytes promoted the expression of inflammatory adipokines (-), giving rise to lower insulin receptor expression and impaired insulin-induced glucose uptake ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
- Not checked yetcites [173] Ehrhart-Bornstein, 2004, Fat cells may be the obesity-hypertension link: human adipogenic factors stimulate aldosterone secretion from adrenocortical cells, Endocr Res source
- Not checked yetcites [174] Rondinone, 1993, Aldosterone stimulated differentiation of mouse 3T3-L1 cells into adipocytes, Endocrinology source
- Not checked yetcites [175] Caprio, 2007, Pivotal role of the mineralocorticoid receptor in corticosteroid-induced adipogenesis, FASEB J source
- Not checked yetcites [176] Guo, 2008, Mineralocorticoid receptor blockade reverses obesity-related changes in expression of adiponectin, peroxisome proliferator-activated receptor-gamma, and proinflammatory adipokines, Circulation source
- Not checked yetcites [177] Lamounier-Zepter, 2006, Fat tissue metabolism and adrenal steroid secretion, Curr Hypertens Rep source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Mineralocorticoids might also indirectly limit insulin secretion by the pancreas as a result of hypokalemia; in other words, impaired insulin secretion could be caused by potassium depletion in individuals with PA.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
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In the paper
“These mechanisms can lead to tissue damage, potentially resulting in altered insulin release and sensitivity ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
- Not checked yetcites [170] Giacchetti, 2005, The renin-angiotensin-aldosterone system, glucose metabolism and diabetes, Trends Endocrinol Metab source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Corticosteroid-binding globulin binds cortisol with a high capacity and affinity, reducing free GC levels to ~%, whereas aldosterone circulates mainly in its free form ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
- Not checked yetcites [163] Funder, 1973, The roles of plasma binding and receptor specificity in the mineralocorticoid action of aldosterone, Endocrinology source
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In the paper
“In patients with primary aldosteronism (PA), resection of aldosteroneproducing tumors and pharmacological treatment both reduced blood insulin and glucose levels, suggesting an improvement in insulin sensitivity (, ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > GC metabolic effects mediated by mineralocorticoid receptors
What the sources say
- Not checked yetcites [167] Giacchetti, 2007, Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study, J Hypertens source
- Not checked yetcites [168] Catena, 2006, Insulin sensitivity in patients with primary aldosteronism: a follow-up study, J Clin Endocrinol Metab source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Fasting plasma glucose (FPG) level may not suffice to assess glucose homeostasis in CS because more than one in two patients (%) with endogenous CS and DM have normal FGP levels () and because an oral glucose tolerance test (OGTT) is not always performed in patients with apparently normal fasting glycemia ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Endogenous CS
What the sources say
- Not checked yetcites [185] Mancini, 2004, High cardiovascular risk in patients with Cushing’s syndrome according to 1999 WHO/ISH guidelines, Clin Endocrinol (Oxf) source
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None of the sources cited for this claim have been checked yet.
In the paper
“No sex-related differences have been described in the prevalence of this CS complication (, ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Endogenous CS
What the sources say
- Not checked yetcites [184] Pecori Giraldi, 2003, Study Group on the Hypothalamo-Pituitary-Adrenal Axis of the Italian Society of Endocrinology. Gender-related differences in the presentation and course of Cushing’s disease, J Clin Endocrinol Metab source
- Not checked yetcites [189] Zilio, 2014, Diagnosis and complications of Cushing’s disease: gender-related differences, Clin Endocrinol (Oxf) source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The risk of DM was greater in subjects with abdominal adiposity or a genetic predisposition to DM and in those taking higher doses of GCs and for longer periods (, -).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Exogenous CS
What the sources say
- Not checked yetcites [194] Gurwitz, 1994, Glucocorticoids and the risk for initiation of hypoglycemic therapy, Arch Intern Med source
- Not checked yetcites [196] Henriksen, 1997, Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients, Diabetologia source
- Not checked yetcites [197] Darmon, 2006, Insulin resistance induced by hydrocortisone is increased in patients with abdominal obesity, Am J Physiol Endocrinol Metab source
- Not checked yetcites [198] Donihi, 2006, Prevalence and predictors of corticosteroid-related hyperglycemia in hospitalized patients, Endocr Pract source
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In the paper
“There is no general consensus, however, on the diagnostic criteria for identifying cases of SCS, which consequently vary considerably among different investigators and studies.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
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In the paper
“By definition, AI patients have no clinical signs of abnormal cortisol secretion; however, % to % of them may have SCS.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
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In the paper
“Generally speaking, the severity of hypercortisolism correlates with the presence of IR and DM, as evidenced by an association with higher urinary free cortisol (UFC) levels (, ), though this was not identified in all studies (, ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Endogenous CS
What the sources say
- Not checked yetcites [181] Friedman, 1996, Carbohydrate and lipid metabolism in endogenous hypercortisolism: shared features with metabolic syndrome X and NIDDM, Endocr J source
- Not checked yetcites [185] Mancini, 2004, High cardiovascular risk in patients with Cushing’s syndrome according to 1999 WHO/ISH guidelines, Clin Endocrinol (Oxf) source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The -mg dexamethasone overnight suppression test is recommended for screening patients with AI for SCS, setting the threshold at nmol/L; a value of nmol/L virtually excludes SCS, whereas values between and nmol/L occupy an area of uncertainty ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
What the sources say
- Not checked yetcites [207] Terzolo, 2002, Adrenal incidentaloma: a new cause of the metabolic syndrome?, J Clin Endocrinol Metab source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Focusing on glucose metabolism, the prevalence of IGT or DM has been higher in patients with SCS than in cases of nonfunctioning adenoma or controls (, , , , , , ), but these data were not confirmed by other studies that found much the same prevalence of these comorbidities in SCS as in the overall series of AI and in the general population (, -).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
What the sources say
- Not checked yetcites [200] Rossi, 2000, Subclinical Cushing’s syndrome in patients with adrenal incidentaloma: clinical and biochemical features, J Clin Endocrinol Metab
- Not checked yetcites [201] Tauchmanovà, 2002, Patients with subclinical Cushing’s syndrome due to adrenal adenoma have increased cardiovascular risk, J Clin Endocrinol Metab source
- Not checked yetcites [203] Terzolo, 2005, Subclinical Cushing’s syndrome in adrenal incidentalomas, Endocrinol Metab Clin North Am source
- Not checked yetcites [207] Terzolo, 2002, Adrenal incidentaloma: a new cause of the metabolic syndrome?, J Clin Endocrinol Metab source
- Not checked yetcites [210] Emral, 2003, Prevalence of subclinical Cushing’s syndrome in 70 patients with adrenal incidentaloma: clinical, biochemical and surgical outcomes, Endocr J source
- Not checked yetcites [211] Morelli, 2010, Subclinical hypercortisolism: correlation between biochemical diagnostic criteria and clinical aspects, Clin Endocrinol (Oxf) source
- Not checked yetcites [220] Morelli, 2014, Long-term follow-up in adrenal incidentalomas: an Italian multicenter study, J Clin Endocrinol Metab source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Overall, DM or IGT was identified in % to % of patients with AI and SCS and was related to patients' age (), the size of their adenomas, their midnight cortisol level, and their plasma cortisol level after suppression with dexamethasone ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
What the sources say
- Not checked yetcites [219] Muscogiuri, 2011, The size of adrenal incidentalomas correlates with insulin resistance. Is there a cause-effect relationship?, Clin Endocrinol (Oxf) source
- Not checked yetcites [211] Morelli, 2010, Subclinical hypercortisolism: correlation between biochemical diagnostic criteria and clinical aspects, Clin Endocrinol (Oxf) source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The results of these studies suggest that chronic mild hypercortisolism, as in SCS, may be associated with the clinical phenotype of IR syndrome or, alternatively, that AI may be per se an unrecognized manifestation of metabolic syndrome.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Subclinical CS
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In the paper
“Ketoconazole has been used worldwide for more than years to lower circulating cortisol levels in CS, although only retrospective studies have reported on its use to date.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Ketoconazole
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“At doses higher than g daily, mitotane also has an adrenolytic effect, inducing cellular necrosis, so it is indicated mainly in adrenal cancer ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > The effect of adrenal-directed drugs
What the sources say
- Not checked yetcites [265] Mancini, 2010, Treatment of Cushing disease: overview and recent findings, Ther Clin Risk Manag source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Available data consequently do not support largescale screening for CS in patients with type DM but may suggest a case-finding approach for hypercortisolism in diabetic patients with certain features (i.e., uncontrolled DM despite appropriate treatment, drug-resistant hypertension, Cushingoid appearance, central obesity, osteoporosis, or polycystic ovary syndrome) (, ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Screening for Hypercortisolism in Patients With Type 2 DM
What the sources say
- Not checked yetcites [245] Leibowitz, 1996, Pre-clinical Cushing’s syndrome: an unexpected frequent cause of poor glycaemic control in obese diabetic patients, Clin Endocrinol (Oxf) source
- Not checked yetcites [263] Nieman, 2008, The diagnosis of Cushing’s syndrome: an Endocrine Society Clinical Practice Guideline, J Clin Endocrinol Metab source
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“As demonstrated by Colao et al. () in , patients cured of CD who have normal serum and urinary cortisol levels for at least years have a higher prevalence of atherosclerosis than healthy controls and maintain several clinical and biochemical abnormalities typical of active CD, such as obesity, hypertension, IGT, hyperlipidemia, and hypercoagulability.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
What the sources say
- Not checked yetcites [191] Colao, 1999, Persistence of increased cardiovascular risk in patients with Cushing’s disease after five years of successful cure, J Clin Endocrinol Metab
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“It is worth noting that no cases of confirmed SCS emerged among a population of diabetic outpatients forming another large series in a recent study in India (); in this study, however, patients with clinical signs suggestive of hypercortisolism (easy bruising, facial plethora, proximal muscle weakness, and/or striae) were excluded a priori from the evaluation.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Screening for Hypercortisolism in Patients With Type 2 DM
What the sources say
- Not checked yetcites [259] Budyal, 2015, Is it worthwhile to screen patients with type 2 diabetes mellitus for subclinical Cushing’s syndrome?, Endocr Connect source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The normalization of cortisol levels after surgery and/or radiotherapy is generally followed by the resolution of patients' glucose metabolism impairment because their hypercortisolism is responsible for their hyperglycemia.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Both treatments can cause hypopituitarism (including GH deficiency) that, left untreated, may alter glucose metabolism and raise patients' cardiovascular risk ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
What the sources say
- Not checked yetcites [266] Gola, 2005, Clinical review: Growth hormone and cardiovascular risk factors, J Clin Endocrinol Metab source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although this figure is too low in absolute terms to support the efficacy of widespread screening, it means that CS is much more common than previously believed, considering the high prevalence of type DM in the general population.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Screening for Hypercortisolism in Patients With Type 2 DM
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“On the other hand, the frequency of CS identified in an unselected population of type DM patients was too low compared with the number of false-positive results to make a routine screening strategy applicable in practice (), given its high cost-effectiveness and the lack of specific tests for diagnosing CS, especially in patients with a slightly elevated cortisol secretion and SCS ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Screening for Hypercortisolism in Patients With Type 2 DM
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Controlling hypercortisolism is the first step toward improving glucose metabolism in patients with endogenous CS, but different treatments for hypercortisolism may affect the outcome of diabetes, regardless of how well cortisol excess is corrected (, , , , , , ).”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
What the sources say
- Not checked yetcites [1] Arnaldi, 2003, Diagnosis and complications of Cushing’s syndrome: a consensus statement, J Clin Endocrinol Metab source
- Not checked yetcites [12] Mazziotti, 2011, Diabetes in Cushing syndrome: basic and clinical aspects, Trends Endocrinol Metab source
- Not checked yetcites [183] Faggiano, 2003, Cardiovascular risk factors and common carotid artery caliber and stiffness in patients with Cushing’s disease during active disease and 1 year after disease remission, J Clin Endocrinol Metab source
- Not checked yetcites [186] Giordano, 2011, Metabolic and cardiovascular outcomes in patients with Cushing’s syndrome of different aetiologies during active disease and 1 year after remission, Clin Endocrinol (Oxf) source
- Not checked yetcites [190] Arnaldi, 2004, Cardiovascular risk in Cushing’s syndrome, Pituitary source
- Not checked yetcites [191] Colao, 1999, Persistence of increased cardiovascular risk in patients with Cushing’s disease after five years of successful cure, J Clin Endocrinol Metab
- Not checked yetcites [264] Baroni, 2016, Italian Society for the Study of Diabetes (SID)/Italian Endocrinological Society (SIE) guidelines on the treatment of hyperglycemia in Cushing’s syndrome and acromegaly, J Endocrinol Invest source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“The remission rate after neurosurgery is in the range of % to %, with a risk of recurrence at years ranging between % and %; for macroadenomas, the remission rate is lower, and recurrences tend to occur earlier than for microadenomas ().”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
What the sources say
- Not checked yetcites [265] Mancini, 2010, Treatment of Cushing disease: overview and recent findings, Ther Clin Risk Manag source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These features mean that patients who have a history of CD carry a higher cardiovascular risk than the general population, albeit lower than in patients with active disease.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Therapeutic Options for CS and Glycemic Control
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Diagnostic tests and cutoffs are important factors influencing the outcome of any screening.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Screening for Hypercortisolism in Patients With Type 2 DM
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- Rests on an assumption: Diagnostic tests and cutoffs are important factors influencing the outcome of any screening.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Because most of the metabolic side effects mediated by GCR are via transactivation, whereas most of the desired anti-inflammatory effects are via transrepression, efforts have been made to separate these two modes of GCR activity.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Selective GCR modulators
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Participation in appetite control a”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Conclusions
What the sources say
- Not checked yetcites a
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Inhibition of prolactin release”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Conclusions
What the sources say
- Not checked yetcites a
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Cortisol is the natural ligand for GCR in humans, and the binding of cortisol or other synthetic GCs results in metabolic and anti-inflammatory effects.”
§ Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management > Selective GCR modulators
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
Glucocorticoids circulate at 100- to 1000-fold higher plasma concentrations than aldosterone.
“MRs have a similar affinity for aldosterone and cortisol (), but GCs circulate at to -fold higher plasma concentrations than does aldosterone.”
The paper relies on this without support.
In brain and adipose tissue, mineralocorticoid receptors are high-affinity glucocorticoid receptors fully occupied by cortisol.
“In other tissues, such as brain and adipose tissue, MRs are considered high-affinity GC receptors, fully occupied by cortisol.”
The paper relies on this without support.
Diagnostic tests and cutoffs are important factors influencing the outcome of any screening.
“Diagnostic tests and cutoffs are important factors influencing the outcome of any screening.”
The paper relies on this without support.
Glucocorticoids induce diabetes mellitus.
“Although GCs are well known to induce DM, no studies have specifically investigated the role of antidiabetic therapy in the treatment of hyperglycemia in patients with endogenous CS, and few studies have reported the effects of some antidiabetic agents in exogenous GC-induced hyperglycemia.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“while diabetes in people with normal CORT levels is characterised by increased fasting glucose, a static metric by all means, secondary diabetes in hypercortisolemic patients can be better characterised by impaired glucose tolerance, a medical test that is intrinsically dynamic ( 14, 15 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“and by stimulating liver gluconeogenesis and glycogenolysis ( 4, 15 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [15]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“This is important in view of the fact that an OGTT may not be performed when a patient's fasting glucose is normal, thus leading to an underestimation of the prevalence of diabetes in hypercortisolism ( 15 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [15]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Incorrect prevalence in the Chiodini screening cohort
MinorThe table reports 30 cases among 294 patients, which is 10.2%, not 9.4%.
Reported 9.4 · recomputed 10.204082
“| Chiodini | 294 | Inpatients, BMI 19-50 kg/m 2 | 1-mg DST (50 nmol/L) | 30 (9.4%) | |”
Citations
Cites
Matthews, D. R., Hosker, J. P., Rudenski, A. S., Naylor, B. A., Treacher, D. F., & Turner, R. C. (1985) · Diabetologia · doi:10.1007/bf00280883 · Cited by 31,502
Diagnosis and Classification of Diabetes Mellitus
American Diabetes Association (2010) · Diabetes Care · doi:10.2337/dc11-s062 · Cited by 14,094
AMPK: a nutrient and energy sensor that maintains energy homeostasis
Hardie, D. G., Ross, F. A., & Hawley, S. A. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3311 · Cited by 4,602
Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., Peters, A. L., Tsapas, A., Wender, R., & Matthews, D. R. (2012) · Diabetologia · doi:10.1007/s00125-012-2534-0 · Cited by 3,919
Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach
Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., Peters, A. L., Tsapas, A., Wender, R., & Matthews, D. R. (2012) · Diabetes Care · doi:10.2337/dc12-0413 · Cited by 3,207
The diagnosis of Cushing's syndrome: an Endocrine Society Clinical Practice Guideline.
Nieman, L. K., Biller, B. M. K., Findling, J. W., Newell-Price, J., Savage, M. O., Stewart, P. M., & Montori, V. M. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-0125 · Cited by 2,718
Endocrine regulation of energy metabolism by the skeleton
Lee, N. K., Sowa, H., Hinoi, E., Ferron, M., Ahn, J. D., Confavreux, C., Dacquin, R., Mee, P. J., McKee, M. D., Jung, D. Y., et al. (2007) · Cell · doi:10.1016/j.cell.2007.05.047 · Cited by 2,554
Diagnosis and classification of diabetes mellitus
American Diabetes Association (2013) · Diabetes Care · doi:10.2337/dc13-s067 · Cited by 2,245
Arriza, J. L., Weinberger, C., Cerelli, G., Glaser, T. M., Handelin, B. L., Housman, D. E., & Evans, R. M. (1987) · Science · doi:10.1126/science.3037703 · Cited by 1,946
Yki-Järvinen, H. (2004) · New England Journal of Medicine · doi:10.1056/nejmra041001 · Cited by 1,830
Flagged first, then by citations
20 of the 383 references couldn’t be matched to a known paper.
Research works printed but not linked: 2
- Boyle, 1993, Cushing’s disease, glucocorticoid excess, glucocorticoid deficiency, and diabetes, Diabetes Res, 1, 301
- 2006, Insulin sensitivity in patients with adrenal incidentaloma [in Serbian], Srp Arh Celok Lek, 134, 315
Cited by
Sorted by citations
Items 101–141 of 141
Diabetic Ketoacidosis and Hyperglycemia
Salam, M., & Liu, J. (2022) · Springer eBooks · doi:10.1007/978-3-030-90225-4_25 · Cited by 2
Serum Cortisol and Cardiovascular Disease Risk - A Potential Biomarker
Oo, W. J., Lim, C. L., Goh, M. H., & Koh, R. Y. (2025) · Current Cardiology Reviews · doi:10.2174/011573403x328499241106064553 · Cited by 1
“Hypercortisolism-induced hyperglycaemia mainly occurs in the liver through the upregulation of enzymes involved in gluconeogenesis and disrupted inhibition of hepatic glucose output [43].”
InfluentialLiao, Y., Zuo, M., Zhu, Y., Xu, T., Tang, J., Fan, L., & Zhang, N. (2025) · Discover Oncology · doi:10.1007/s12672-025-02108-y · Cited by 1
“…excess visceral adipose tissue is closely related to insulin resistance, and its secretion of a variety of adipokines and inflammatory mediators, such as free fatty acids and TNF-α, interferes with insulin signaling pathways, reduces insulin sensitivity, and exacerbates insulin resistance [23].”
Glukosestoffwechsel aus dem Lot? Auch endokrinologische Ursachen abklären!
Müssig, K. (2025) · Info Diabetologie · doi:10.1007/s15034-025-5112-5 · Cited by 1
Lipodystrophy look-alikes: navigating diagnostic overlap with endocrine diseases
Ceccarini, G., Gilio, D., Magno, S., Palladino, L., & Santini, F. (2026) · European Journal of Endocrinology · doi:10.1093/ejendo/lvag067 · Cited by 2
Chasan, O., Terzioglu, M. B. B., Mutlu, Ü., Burak, D. D., Hacışahinoğulları, H., Gül, N., Selçukbiricik, Ö. S., Üzüm, A. K., & Yalın, G. Y. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1798032 · Cited by 2
Cardiac Natriuretic Peptide System: A Link between Adipose Tissue, Obesity, and Insulin Resistance
Öztop, M. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.104560 · Cited by 1
Metabolic status in children with Cushing’s disease and its relationship with remission
Moszczyńska, E., Baszyńska–Wilk, M., Bogusz-Wójcik, A., Pasternak-Pietrzak, K., Mazur, M., & Wysocka‐Mincewicz, M. (2023) · Pediatric Endocrinology Diabetes and Metabolism · doi:10.5114/pedm.2023.130026 · Cited by 1
“Correction of cortisol level after TSS is generally followed by improved glucose metabolism [32].”
BackgroundAlkwatli, K., Kodali, A. M., & Pantalone, K. M. (2024) · Endocrine Practice · doi:10.1016/j.eprac.2024.02.003 · Cited by 1
Steroiddiabetes: Risiken, Diagnostik und Handlungsstrategien
Gallwitz, B. (2025) · Info Diabetologie · doi:10.1007/s15034-025-5113-4 · Cited by 1
“%) der Fälle liegt ein manifester Diabetes mellitus vor [14].”
Araya, A. V., Liberman, C., Munizaga, C., Pineda, P., Marcela Barberán, M., Cordero, F., Lanas, A., & Toro, L. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.106521 · Cited by 1
Therapy of mild cortisol excess
Iqbal, A., & Newell-Price, J. D. C. (2019) · Current Opinion in Endocrine and Metabolic Research · doi:10.1016/j.coemr.2019.08.019
Analysis of Clinical Characteristics of Glucose Metabolism in 118 Patients with Cushing’s Syndrome
怀, 宙. (2021) · Advances in Clinical Medicine · doi:10.12677/acm.2021.113142
Hillson, R. (2022) · Practical Diabetes · doi:10.1002/pdi.2372
Schernthaner-Reiter, M. H., Wolf, P. S., Vila, G., & Luger, A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819949-7.00037-8 · Cited by 1
Non dimentichiamo l’anamnesi e la fisiologia
Ceccato, F. (2022) · L Endocrinologo · doi:10.1007/s40619-022-01191-5
Gestione delle alterazioni del metabolismo glucidico nell’acromegalia e nella malattia di Cushing
Voltan, G., Scaroni, C. M., & Ceccato, F. (2023) · L Endocrinologo · doi:10.1007/s40619-023-01288-5
“A livello del tessuto adiposo viscerale i glucocorticoidi promuovono la differenziazione dei pre-adipociti in adipociti maturi, incrementano la lipolisi e la produzione di adipochine quali la leptina [1].”
BackgroundSelf-citationClinical manifestations of functionally autonomous cortisol secretion in patients with adrenal masse
Chzhen, T. R., & Киселева, Т. П. (2023) · Ural Medical Journal · doi:10.52420/2071-5943-2023-22-3-13-21
Ashraf, S., Parveen, S., Ashraf, S., Batool, U., Sultana, M., Ishaque, U., Shafqat, Z., Shabbir, S., Riaz, Z., & Faiz, Z. (2023) · BioScientific Review · doi:10.32350/bsr.52.04
“Glucose metabolism should be subsequently monitored and properly targeted for glycemic control as in diabetic patients, even though their fasting glucose levels remain normal [11].”
BackgroundLlavero-Valero, M., Vaamonde, J., & Buey, G. G. (2023) · Medicine - Programa de Formación Médica Continuada Acreditado · doi:10.1016/j.med.2023.12.002
Long-term complications of hypercortisolism
Pivonello, R., Crescenzo, E. M., Simeoli, C., Paola, N. D., Larocca, A., & Colao, A. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-13825-6.00123-0
(2000) · Time to knit · doi:10.1016/s1155-1941(19)82702-6
Đặc điểm rối loạn chuyển hoá ở trẻ mắc hội chứng cushing do sử dụng glucocorticoids
Khánh, N. N., & Ngọc, C. T. B. (2025) · Tạp chí Nghiên cứu Y học · doi:10.52852/tcncyh.v191i6.3548
Wang, M., Li, S., Cui, Q., Huang, B., & Cui, J. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1678472
“The prevalence of diabetes mellitus and impaired glucose tolerance in patients with CS is 20% to 45% and 10% to 30%, respectively, so the overall prevalence of abnormal glucose metabolism is close to 70% (39).”
Liu, Y., Zhang, P., Zhang, S., Gao, Y., Mu, Y., Lian, H., Ren, Q., Cai, X., Zhou, X., Han, X., et al. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1663619
New Diagnosis of Adrenocortical Carcinoma with Stroke Workup
Zhu, R., Tshimbombu, T. N., Rodriguez, M. C., Gil, M. M., Yuen, K. C. J., & Banyas, P. (2025) · Case Reports in Neurology · doi:10.1159/000549473
“Studies have shown that up to 70% of CS patients have glucose metabolism impairments [12], 80% have hypertension [13] and 72% have dyslipidemia [14].”
Hsiao, I.-T., & Lu, C.-H. (2026) · Cureus · doi:10.7759/cureus.103162
Chasseloup, F. (2022) · theses.fr (ABES) · doi:10.70675/ddec5b6dzf376z4aadz9970zf0bf052c6f02
Morgante, C., Cammà, C., PETTA, S., Guarnotta, V., & Arnaldi, G. (2026) · World Journal of Gastroenterology · doi:10.3748/wjg.v32.i16.116142
Bei schwer einstellbarem Typ-2-Diabetes an Hyperkortisolismus denken
Müssig, K. (2026) · Info Diabetologie · doi:10.1007/s15034-026-5260-2
Martínez, W. A. R., Builes-Montaño, C. E., Román-González, A., Barrera, C. A. B., Castaño, M. J. R., & Gutiérrez-Restrepo, J. (2026) · Vitamins and hormones · doi:10.1016/bs.vh.2026.03.002
Cushing´s syndrome: Clinical presentation and associated comorbidities
Abreu-Lomba, A., Salazar-Solarte, A. M., Trujillo, D. A. V., & Martínez, W. A. R. (2026) · Vitamins and hormones · doi:10.1016/bs.vh.2026.04.001
Altıntaş, M., & Özmen, Ö. (2026) · Hormone and Metabolic Research · doi:10.1055/a-2885-1938
Hypercortisolism: Causes, Consequences and Clinical Significance – A Review of Pathophysiology
Eldib, M., Fierro, F. E., Abad, M. O., & Correa, R. R. (2026) · Diabetes Obesity and Metabolism · doi:10.1111/dom.71022 · Cited by 1
Bitaraf, M., & Memarian, M. (2026) · Journal of Preventive Epidemiology · doi:10.34172/jpe.39326
Metabolomics and Metabolic Endocrine Diseases
Zheng, X., Kuang, J., Ren, J., Cai, Y., & Xia, L. (2026) · Springer eBooks · doi:10.1007/978-981-95-9567-9_2
Insulin resistance beyond adiposity: Recognizing non-obese phenotypes
Shaooli, R. C. (2026) · Obesity Medicine · doi:10.1016/j.obmed.2026.100736
Hypercortisolism: An Under‐Recognised Pathway Linked to Multi‐System Complications
Sacoto, H. D., & Fonseca, V. A. (2026) · Diabetes Obesity and Metabolism · doi:10.1111/dom.71149
“This is thought to be the result of a mechanism involving genomic and non-genomic glucocorticoid receptor (GR) pathways [37, 42].”
Velasco-López, J. A., Martínez, J. J. A., Martínez, M. G., Jiménez-Martínez, C., Moya, A. J. M., & Lamas, C. (2026) · Endocrinología Diabetes y Nutrición · doi:10.1016/j.endinu.2026.501904
WITEK, P. W., Kwiatkowski, J., Witek, J., Szamotulska, K., & Zieliński, G. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1941836
Metadata
- Authors
- Scaroni, C., Zilio, M., Foti, M., & Boscaro, M.
- Affiliations
- University of Padua (IT)
- Department of Cell Physiology & Metabolism, Centre Médical Universitaire, 1 Rue Michel Servet, 1211 Genèva, Switzerland
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2017-03-20
- Volume
- 38
- Issue
- 3
- Pages
- 189-219
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2621858797
- Semantic Scholar
- 8c0496e85c53fd1dd9e21c5d85f1fdab54f725cc
- Cited by
- 140
- References
- 383
- Citations by year
- 2026: 16 · 2025: 20 · 2024: 13 · 2023: 17 · 2022: 19 · 2021: 21 · 2020: 14 · 2019: 12 · 2018: 5 · 2017: 2
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, cc-by)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- Eli Lilly and Company
- Pfizer
- Viropharma
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Keywords
- Cushing's syndrome, glucose metabolism, hypercortisolism, glucocorticoid excess, diabetes mellitus, glucose homeostasis, subclinical Cushing's syndrome, glycemic control
- MeSH terms
- Animals, Blood Glucose, Cushing Syndrome, Glucocorticoids, Humans, Hydrocortisone, Insulin Resistance, Signal Transduction, Glucose Metabolism Disorders
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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