The DOI matches its Crossref record; 223 of the 223 references it cites were found in a registry or an index; 13 of the 100 sources its claims cite were checked for support.
Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future
Open accessAbstract
Glucose metabolism is normally regulated by a feedback loop including islet β cells and insulin-sensitive tissues, in which tissue sensitivity to insulin affects magnitude of β-cell response. If insulin resistance is present, β cells maintain normal glucose tolerance by increasing insulin output. Only when β cells cannot release sufficient insulin in the presence of insulin resistance do glucose concentrations rise. Although β-cell dysfunction has a clear genetic component, environmental changes play an essential part. Modern research approaches have helped to establish the important role that hexoses, aminoacids, and fatty acids have in insulin resistance and β-cell dysfunction, and the potential role of changes in the microbiome. Several new approaches for treatment have been developed, but more effective therapies to slow progressive loss of β-cell function are needed. Recent findings from clinical trials provide important information about methods to prevent and treat type 2 diabetes and some of the adverse effects of these interventions. However, additional long-term studies of drugs and bariatric surgery are needed to identify new ways to prevent and treat type 2 diabetes and thereby reduce the harmful effects of this disease.
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Claims the paper makes
67 Not checked yet · 10 Own interpretation · 4 No basis given · 2 Partly supported · 1 Couldn’t confirm · accuracy not yet measured
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In none of these studies did intensive glucose lowering reduce cardiovascular events”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Could not verifycites [121] Tolhurst, 2012, Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2, Diabetes sourceExperimental — accuracy not yet measured
The Results section on FFAR2 and FFAR3 reports GLP-1 secretion and glucose tolerance in mice, not cardiovascular events in clinical trials (page unavailable). Searches for ACCORD, VADT, ORIGIN, ADVANCE, and intensive glycemic control found no passage in our copy addressing the claimed trial outcomes. (LLM, conf=0.76)
- Could not verifycites [122] El Ouaamari, 2013, Liver-derived systemic factors drive β cell hyperplasia in insulin-resistant states, Cell Rep sourceExperimental — accuracy not yet measured
The Results and Discussion passage concerns glucose levels and β-cell proliferation in mice, not cardiovascular outcomes. Searches for ACCORD, VADT, ORIGIN, ADVANCE, and intensive glucose lowering found no passage in our copy addressing those trials or their cardiovascular results; page numbers were not available. (LLM, conf=0.75)
- Could not verifycites [123] Yi, 2013, Betatrophin: a hormone that controls pancreatic β cell proliferation, Cell sourceExperimental — accuracy not yet measured
The Results section discusses insulin resistance and β-cell proliferation in mice, while the Experimental Procedures describe glucose-tolerance testing in mice. Searches for ACCORD, VADT, ORIGIN, ADVANCE, and cardiovascular outcomes found no passage in our copy addressing whether intensive glucose lowering reduced cardiovascular events in those trials. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
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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
“When insulin resistance is present, as seen most commonly with obesity, the β-cell increases its insulin output to maintain normal glucose tolerance (Figure 1B).”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“a proportion of these abnormalities are explained by adiposity, especially that located within the intra-abdominal cavity6.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Past: Identification of β-cell Dysfunction and Insulin Resistance
What the sources say
- Not checked yetcites [6] Cnop, 2002, The concurrent accumulation of intra-abdominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations: distinct metabolic effects of two fat compartments, Diabetes source
plainconditional- Asserted: passes — The authors put it forward as true.
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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
“However, when the β-cell is incapable of this task, the result is an elevation in plasma glucose (Figure 1C).”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Insulin resistance is already well established when impaired glucose tolerance is present”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
What the sources say
- Not checked yetcites [9] Stancáková, 2009, Changes in insulin sensitivity and insulin release in relation to glycemia and glucose tolerance in 6,414 Finnish men, Diabetes source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Further, it has been shown that β-cell function is heritable16 and critically determines glucose intolerance and type 2 diabetes in different racial and ethnic groups17.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
What the sources say
- Not checked yetcites [16] Elbein, 1999, Heritability of pancreatic beta-cell function among nondiabetic members of Caucasian familial type 2 diabetic kindreds, J Clin Endocrinol Metab
boosted- Asserted: passes — The authors put it forward as true.
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In the paper
“The worldwide explosion of obesity has resulted in an ever-increasing prevalence of type 2 diabetes”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Type 2 Diabetes: The Epidemic of Our Time
What the sources say
- Not checked yetcites [1]
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This feedback loop relies on crosstalk between the β-cell and the insulin sensitive tissues (Figure 1A).”
- Also stated in: § The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis · plain
“a feedback loop operates to ensure integration of glucose homeostasis and maintenance of glucose in a tight range7.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
What the sources say
- Not checked yetcites [7] Kahn, 1993, Quantification of the relationship between insulin sensitivity and β-cell function in human subjects: evidence for a hyperbolic function, Diabetes source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Diminished β-cell function is already present in groups known to be at increased risk of diabetes including first-degree relatives of individuals with diabetes12, women with gestational diabetes13 or polycystic ovary syndrome14 and older individuals15 and underlies the progression to diabetes.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
What the sources say
- Not checked yetcites [12] Cnop, 2007, Progressive loss of β-cell function leads to worsening glucose tolerance in first-degree relatives of subjects with type 2 diabetes, Diabetes Care source
- Not checked yetcites [13] Ward, 1985, Insulin resistance and impaired insulin secretion in subjects with histories of gestational diabetes mellitus, Diabetes source
- Not checked yetcites [14] Dunaif, 1996, Beta-cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome, J Clin Endocrinol Metab
- Not checked yetcites [15] Kahn, 1992, Exercise training delineates the importance of B-cell dysfunction to the glucose intolerance of human aging, J Clin Endocrinol Metab
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Further progressive deterioration of β-cell function accounts for the evolving natural history of the disease from impaired glucose tolerance to type 2 diabetes10,11.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
What the sources say
- Not checked yetcites [10] Weyer, 1999, The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus, J Clin Invest source
- Not checked yetcites [11] Kahn, 2011, Effects of rosiglitazone, glyburide, and metformin on β-cell function and insulin sensitivity in ADOPT, Diabetes source
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 32
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Together these genes do not appear to explain much of the genetic basis of the disease with the use of genotype risk scores only slightly improving prediction of subsequent diabetes compared to common clinical risk factors22,23.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Genes, Environment and the Development of Type 2 Diabetes
What the sources say
- Supportedcites [22] Meigs, 2008, Genotype score in addition to common risk factors for prediction of type 2 diabetes, N Engl J Med source
The Discussion says the 18 SNPs account for a minority of diabetes heritability. It also concludes that the genotype score did not substantially improve prediction beyond common phenotypic risk factors. (LLM, conf=0.93)
- Partly supportedcites [23] Lyssenko, 2008, Clinical risk factors, DNA variants, and the development of type 2 diabetes, N Engl J Med sourceExperimental — accuracy not yet measured
The Abstract and Discussion report that adding known DNA variants to clinical risk factors only slightly improved prediction of future type 2 diabetes (AUC 0.74 to 0.75). The paper also reports low discriminatory power for the genes alone, but it does not establish how much of the disease’s genetic basis these genes explain. (LLM, conf=0.83)
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These trials have more or less uniformly demonstrated a benefit, with lifestyle more efficacious than all medications with the exception of the thiazolidinediones140–152.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [140] Gathercole, 2013, 11β-hydroxysteroid dehydrogenase 1: translational and therapeutic aspects, Endocr Rev source
- Could not verifycites [141] Tschöp, 2012, Outstanding Scientific Achievement Award Lecture 2011: defeating diabesity: the case for personalized combinatorial therapies, Diabetes sourceExperimental — accuracy not yet measured
The challenge section discusses the difficulty of sustaining weight loss through diet or exercise and of developing effective drugs, but it does not compare interventions for delaying diabetes onset. Searches for the lifestyle-versus-medication comparison and thiazolidinediones found no passage in our copy addressing that claim. (LLM, conf=0.72)
- Could not verifycites [142] Tan, 2013, Coadministration of glucagon-like peptide-1 during glucagon infusion in humans results in increased energy expenditure and amelioration of hyperglycemia, Diabetes sourceExperimental — accuracy not yet measured
The Research Design and Methods and Discussion passages describe an acute GLP-1 and glucagon infusion study in volunteers without diabetes, not trials to delay diabetes onset. Searches for lifestyle interventions, diabetes-prevention trials, and thiazolidinediones found no passage comparing lifestyle with medications. (LLM, conf=0.77)
- Not checked yetcites [143] 1998, Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33), Lancet source
- Not checked yetcites [144] Gerstein, 2008, Effects of intensive glucose lowering in type 2 diabetes, N Engl J Med source
- Could not verifycites [145] Duckworth, 2009, Glucose control and vascular complications in veterans with type 2 diabetes, N Engl J Med sourceExperimental — accuracy not yet measured
The Treatment Protocol and Discussion (page unavailable) concern glucose control and vascular outcomes in veterans who already had type 2 diabetes. Searches for lifestyle interventions, delayed diabetes onset, and comparisons with thiazolidinediones found no passage addressing the claimed prevention-trial results. (LLM, conf=0.76)
- Partly supportedcites [146] Gerstein, 2012, Basal insulin and cardiovascular and other outcomes in dysglycemia, N Engl J Med sourceExperimental — accuracy not yet measured
The Other Outcomes section reports fewer new diabetes cases with insulin glargine than with standard care, supporting benefit for one drug intervention. The paper does not establish that lifestyle interventions outperform medications other than thiazolidinediones, or that the trials were generally beneficial; searches for lifestyle comparisons and thiazolidinediones found no such passage. Page numbers were not available in our copy. (LLM, conf=0.84)
- Could not verifycites [147] Patel, 2008, Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes, N Engl J Med sourceExperimental — accuracy not yet measured
The Methods (p. 2) study glucose control in people who already have type 2 diabetes, and the Conclusions (p. 2) report vascular outcomes. Searches for lifestyle interventions to delay diabetes onset and comparisons with thiazolidinediones found no passage addressing the claimed relative efficacy. (LLM, conf=0.76)
- Could not verifycites [148] Riddle, 2010, Epidemiologic relationships between A1C and all-cause mortality during a median 3·4-year follow-up of glycemic treatment in the ACCORD trial, Diabetes Care sourceExperimental — accuracy not yet measured
The Research Design and Methods section describes an ACCORD trial in people who already had type 2 diabetes, comparing intensive and standard glycemic targets; it mentions lifestyle interventions but does not compare them with medications. Searches for diabetes-onset prevention, lifestyle efficacy, and thiazolidinediones found no passage addressing the claimed comparison. (LLM, conf=0.77)
- Could not verifycites [149] Ismail-Beigi, 2010, Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial, Lancet sourceExperimental — accuracy not yet measured
The Introduction and Methods describe ACCORD as a trial of intensive versus standard glycaemic treatment in people who already had type 2 diabetes; its stated outcomes were microvascular complications. Searches for diabetes-onset prevention and for a lifestyle-versus-thiazolidinedione comparison found no passage addressing the claim. Page numbers were not available in our copy. (LLM, conf=0.74)
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Further analyses from TODAY show that in youth with type 2 diabetes dyslipidaemia162 and hypertension163 are common and worsen over time.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Could not verifycites [162] Bunck, 2011, Effects of exenatide on measures of β-cell function after 3 years in metformin-treated patients with type 2 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Conclusions discuss exenatide, insulin glargine and β-cell function over three years, not TODAY findings in youth. Searches for TODAY, youth, dyslipidaemia and hypertension found no passage addressing whether those conditions are common or worsen over time. (LLM, conf=0.76)
- Not checked yetcites [163] Pan, 1997, Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study, Diabetes Care source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Could not verify
In the paper
“individuals with “early maturity onset diabetes” produced insulin and secreted this hormone in response to nutrient ingestion2.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Past: Identification of β-cell Dysfunction and Insulin Resistance
What the sources say
- Not checked yetcites [2] Yalow, 1960, Immunoassay of endogenous plasma insulin in man, J Clin Invest source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“this contributed to increased glucose production by the liver and decreased glucose uptake in muscle and adipose tissue5.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Past: Identification of β-cell Dysfunction and Insulin Resistance
What the sources say
- Not checked yetcites [5] Reaven, 1988, Banting lecture 1988. Role of insulin resistance in human disease, Diabetes source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It 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 reality is that these disturbances are a continuum in which the magnitude of the reduction in β-cell function determines the degree of elevation in plasma glucose.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The basis for this loss is multifactorial, and includes glucolipotoxicity32 and amyloid deposition that result in β-cell apoptosis through oxidative as well as endoplasmic reticulum stress31.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Further Delineation of the Roles of Reduced β-cell Number and α-cell Dysfunction
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“While a few loci are associated with obesity and insulin resistance, the vast majority are linked to the β-cell21.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Genes, Environment and the Development of Type 2 Diabetes
What the sources say
- Not checked yetcites [21] McCarthy, 2010, Genomics, type 2 diabetes, and obesity, N Engl J Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It 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
“it is clear that the disease process is heterogeneous, including other pathogenic factors discussed subsequently.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Feedback Regulation Identifies the Critical Role of the β-cell in Glucose Homeostasis
boosted- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Obesity is frequently characterized by systemic inflammation and preclinical evidence links systemic inflammation to β-cell dysfunction63,64.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Systemic and Islet Inflammation
What the sources say
- Not checked yetcites [63] Dula, 2010, Evidence that low-grade systemic inflammation can induce islet dysfunction as measured by impaired calcium handling, Cell Calcium source
- Not checked yetcites [64] Nicol, 2013, Pancreatic inflammation and increased islet macrophages in insulin-resistant juvenile primates, J Endocrinol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“They are endogenous ligands of the farnesoid X receptor (FXR), their activation of FXR resulting in the release of fibroblast growth factor (FGF) 1943.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Important Roles of the Intestine and Brain
What the sources say
- Not checked yetcites [43] Potthoff, 2012, Endocrine fibroblast growth factors 15/19 and 21: from feast to famine, Genes Dev source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“GLP-1 is the more important of these hormones acting on both β- and α-cells to enhance insulin and suppress glucagon secretion, respectively37.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Important Roles of the Intestine and Brain
What the sources say
- Not checked yetcites [37] Drucker, 2006, The biology of incretin hormones, Cell Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Direct effects of inflammation on β-cells arise from activation of the intra-islet immune response, the strongest support being for a role for interleukin-1β (IL-1β)71.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Pathogenesis of Type 2 Diabetes: From Past to Present Day and the Future > The Present: Systemic and Islet Inflammation
What the sources say
- Not checked yetcites [71] Donath, 2003, Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes, J Mol Med (Berl) source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Analyses from ACCORD suggest that the individual likely to be at greatest risk of an adverse outcome to aggressive glucose lowering had a longer duration of diabetes, poor glucose control at the time of commencing intensive insulin therapy, and did not demonstrate an immediate glucose lowering response125.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [125] Gelling, 2003, Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice, Proc Natl Acad Sci USA source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Despite differential weight loss for over 10 years and improvements in many cardiovascular risk factors, including blood pressure and lipids, lifestyle change did not reduce cardiovascular events compared to diabetes support and education (control)133.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [133] Adams, 2013, LY2405319, an engineered FGF21 variant, improves the metabolic status of diabetic monkeys, PLoS One source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“consistent with the multifactorial approach in the Steno 2 Study that demonstrated a reduction in both cardiovascular and microvascular events which was sustained even after cessation of the initial glucose, blood pressure and lipid lowering regimens132.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [132] Kliewer, 2010, Fibroblast growth factor 21: from pharmacology to physiology, Am J Clin Nutr source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Such a microvascular benefit was also shown in ADVANCE, the magnitude being related to the degree of glucose control and affecting largely renal outcomes (essentially a reduction in microalbuminuria)124.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [124] Talchai, 2012, Pancreatic β cell dedifferentiation as a mechanism of diabetic β cell failure, Cell source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“Thus, based on five separate studies, it would seem that current approaches involving intensification of glucose control are valuable for reducing microvascular complications but are not effective in reducing cardiovascular events, possibly even being harmful in those with advanced type 2 diabetes.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“This may have been because large proportions of subjects in both groups received medical treatment for these risk factors.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
In the paper
“serum from type 2 diabetic patients treated with glargine activates insulin receptors A and B similarly to NPH insulin and does not increase signalling through the IGF-1 receptor128.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [128] Agius, 2007, New hepatic targets for glycaemic control in diabetes, Best Pract Res Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Whereas the onset of glucose lowering with the other two medications was slower, it was most sustained with rosiglitazone, with metformin demonstrating an intermediate pattern.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [138] Lindsay, 2003, Subcutaneous adipose 11 beta-hydroxysteroid dehydrogenase type 1 activity and messenger ribonucleic acid levels are associated with adiposity and insulinemia in Pima Indians and Caucasians, J Clin Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Glibenclamide produced the greatest initial reduction in glycaemia, but was poorest in maintaining glucose control.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [138] Lindsay, 2003, Subcutaneous adipose 11 beta-hydroxysteroid dehydrogenase type 1 activity and messenger ribonucleic acid levels are associated with adiposity and insulinemia in Pima Indians and Caucasians, J Clin Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“Thus, intensive lifestyle change in patients with type 2 diabetes has benefits, but unfortunately not on cardiovascular outcomes which remain the major determinant of premature mortality in type 2 diabetes.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Cardiovascular outcomes remain the major determinant of premature mortality in type 2 diabetes.
None of the sources cited for this claim have been checked yet.
In the paper
“Both microalbuminuria and retinopathy increase with diabetes duration and severity is related to glycaemic control163,164.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [163] Pan, 1997, Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study, Diabetes Care source
- Not checked yetcites [164] Tuomilehto, 2001, Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The results of SAVOR-TIMI 53 (NCT01107886) and EXAMINE (NCT00968708) were recently released and showed no increased risk of cardiovascular events with the DPP-4 inhibitors saxagliptin96 and alogliptin97, respectively.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > What Does the Future Hold and Need?
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The disease’s course in youth appears to be more aggressive than in adults, with the differential impact of the interventions being the result of a greater improvement in β-cell function160.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [160] Rejeski, 2012, Lifestyle change and mobility in obese adults with type 2 diabetes, N Engl J Med source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While the number of pancreas-related events in SAVOR-TIMI 53 and EXAMINE were too small to be definitive, there was no evidence for a marked excess of such events with either medication.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > What Does the Future Hold and Need?
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, despite good rationale for approval of interventions to delay the onset of diabetes159, no medication has yet received official sanction as a preventative treatment.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [159] Foster, 2009, A randomized study on the effect of weight loss on obstructive sleep apnea among obese patients with type 2 diabetes: the Sleep AHEAD study, Arch Intern Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“The pathogenesis of the syndrome in children is also critically determined by β-cell function loss with the degree of residual β-cell function determining glucose control in recently diagnosed patients160.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [160] Rejeski, 2012, Lifestyle change and mobility in obese adults with type 2 diabetes, N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The TODAY (Treatment Options for Type 2 Diabetes in Adolescents and Youth) study examined the impact of lifestyle and medications in a young cohort with diabetes duration of less than a year and found glycaemia to be best managed by the combination of rosiglitazone and metformin, with the addition of lifestyle to metformin being no better than metformin alone161.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > Where Do We Stand Today?
What the sources say
- Not checked yetcites [161] Kahn, 2006, Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy, N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
“Given that current treatment approaches do not prevent or slow the loss of β-cell function, there is clearly an urgent need for alternative approaches.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > What Does the Future Hold and Need?
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Type 2 diabetes is a progressive disease driven by advancing β-cell dysfunction.
In the paper
“While current treatment algorithms are less prescriptive than before and advocate a more personalized approach to the choice of medications and treatment targets for type 2 diabetes131”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > What Does the Future Hold and Need?
What the sources say
- Not checked yetcites [131] Ma, 2011, PTP1B inhibitor improves both insulin resistance and lipid abnormalities in vivo and in vitro, Mol Cell Biochem source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, these hypotheses are based on results from the Swedish Obese Subjects Study in which subjects were not randomized and the control group was contemporaneously matched, only received conventional treatment, and differed by a number of characteristics at baseline.”
§ PATHOPHYSIOLOGY AND TREATMENT OF TYPE 2 DIABETES: PERSPECTIVES ON THE PAST, PRESENT AND FUTURE > Treatment and Prevention: Goals and Outcomes of Clinical Trials > What Does the Future Hold and Need?
What the sources say
- Not checked yetcites [173] Gerstein, 2006, Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial, Lancet source
- Not checked yetcites [174] DeFronzo, 2011, Pioglitazone for diabetes prevention in impaired glucose tolerance, N Engl J Med source
- Not checked yetcites [175] Zinman, 2010, Low-dose combination therapy with rosiglitazone and metformin to prevent type 2 diabetes mellitus (CANOE trial): a double-blind randomised controlled study, Lancet source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
The human gene pool has not changed in recent times.
“As our gene pool has not changed in recent times, environmental changes have been critical in determining the type 2 diabetes epidemic.”
The paper relies on this without support.
The reduction in β-cell mass in type 2 diabetes is insufficient to explain the degree of impairment in insulin release.
“While a reduction in β-cell mass exists in type 2 diabetes, it is clear that the magnitude of this abnormality is insufficient to explain the degree of impairment in insulin release.”
The paper relies on this without support.
The current treatment armamentarium does not readily attain and maintain normal glucose levels as β-cell function progressively declines.
“As the current treatment armamentarium does not readily attain and maintain normal glucose levels as β-cell function progressively declines, new and novel approaches are being developed.”
The paper relies on this without support.
Type 2 diabetes is a progressive disease driven by advancing β-cell dysfunction.
“As type 2 diabetes is a progressive disease due to advancing β-cell dysfunction”
The paper relies on this without support.
People with impaired glucose tolerance and/or impaired fasting glucose are at high risk of developing type 2 diabetes.
“Slowing disease progression has also focused on individuals with impaired glucose tolerance and/or impaired fasting glucose because of their high risk of developing type 2 diabetes.”
The paper relies on this without support.
Current treatment algorithms are based largely on industry-conducted studies that typically compare no more than two medications and are short term.
“Current treatment algorithms are based largely on industry-conducted studies, which typically do not compare more than two medications and are short term.”
The paper relies on this without support.
Cardiovascular outcomes remain the major determinant of premature mortality in type 2 diabetes.
“which remain the major determinant of premature mortality in type 2 diabetes.”
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?
In the citing paper
“Its onset is primarily driven by weight gain to an excessive level for that individual, in a complex disease process involving gut hormones, low-grade inflammation and metabolites, possibly including some from the gut microbiota [1].”
In the citing paper
“Type 2 diabetes (T2D), which has currently become a global pandemic, is a metabolic disease largely characterised by impaired insulin secretion and action.”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [5]
In the citing paper
“T2D is largely caused by impaired insulin production and secretion by pancreatic beta-cells, as well as peripheral tissue insulin resistance.5,6”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [5]
Citations
Cites
1 retracted
RETRACTED: Betatrophin: A Hormone that Controls Pancreatic β Cell Proliferation
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RetractedReduction in the incidence of type 2 diabetes with lifestyle intervention or metformin
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Metadata
- Authors
- Kahn, S. E., Cooper, M. E., & Del Prato, S.
- Affiliations
- University of Washington (US)
- Baker Heart and Diabetes Institute (AU)
- Corresponding author
- Kahn, Steven E
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 383
- Issue
- 9922
- Pages
- 1068-1083
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC4226760
- OpenAlex
- W2153399820
- Cited by
- 1,743
- References
- 223
- Citations by year
- 2026: 88 · 2025: 129 · 2024: 141 · 2023: 162 · 2022: 159 · 2021: 184 · 2020: 169 · 2019: 157 · 2018: 151 · 2017: 123 · 2016: 137 · 2015: 97 · 2014: 41
- FWCI
- 13.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- National Institutes of Health (DK-017047)
- U.S. Department of Veterans Affairs
- National Health and Medical Research Council (2010YK7Z5K_006)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- type 2 diabetes, insulin resistance, beta-cell dysfunction, glucose metabolism, insulin secretion, glucose tolerance, gut microbiota, fatty acids, amino acids, hexoses, diabetes prevention, diabetes treatment, bariatric surgery
- MeSH terms
- Diabetes Mellitus, Type 2, Glucose, Humans, Inflammation, Insulin, Insulin Resistance, Obesity, Genetic Predisposition to Disease, Epigenesis, Genetic, Bariatric Surgery, Glucagon-Secreting Cells, Insulin-Secreting Cells, Gene-Environment Interaction
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 2026-10-05, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
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Statistics and arithmetic are recomputed, not judged.
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