The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index; none of the 56 sources its claims cite is checked for support yet.
Leptin in humans: lessons from translational research
Open accessAbstract
Leptin has emerged over the past decade as a key hormone in not only the regulation of food intake and energy expenditure but also in the regulation of neuroendocrine and immune function as well as the modulation of glucose and fat metabolism as shown by numerous observational and interventional studies in humans with (complete) congenital or relative leptin deficiency. These results have led to proof-of-concept studies that have investigated the effect of leptin administration in subjects with complete (congenital) leptin deficiency caused by mutations in the leptin gene as well as in humans with relative leptin deficiency, including states of lipoatrophy or negative energy balance and neuroendocrine dysfunction, as for instance seen with hypothalamic amenorrhea in states of exercise-induced weight loss. In those conditions, most neuroendocrine, metabolic, or immune disturbances can be restored by leptin administration. Leptin replacement therapy is thus a promising approach in several disease states, including congenital complete leptin deficiency, states of energy deprivation, including anorexia nervosa or milder forms of hypothalamic amenorrhea, as well as syndromes of insulin resistance seen in conditions such as congenital or acquired lipodystrophy. In contrast, states of energy excess such as garden-variety obesity are associated with hyperleptinemia that reflects either leptin tolerance or leptin resistance. For those conditions, development of leptin sensitizers is currently a focus of pharmaceutical research. This article summarizes our current understanding of leptin's role in human physiology and its potential role as a novel therapeutic option in human disease states associated with a new hormone deficiency, ie, leptin deficiency.
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TL;DR
This review synthesizes observational and interventional human studies showing that leptin is a key hormone regulating food intake, energy expenditure, neuroendocrine axes, immune function, and glucose/fat metabolism, with its major physiologic role being to signal inadequate rather than excess energy stores. Leptin replacement therapy restores neuroendocrine, metabolic, and immune function in states of absolute or relative leptin deficiency, whereas states of energy excess (garden-variety obesity) are characterized by hyperleptinemia reflecting leptin tolerance or resistance.
Key findings
- Leptin, a 167-amino acid peptide primarily expressed in adipose tissue, circulates in free (biologically active) form and is secreted in a pulsatile, diurnal-nocturnal pattern; pulse amplitude is higher in obese subjects, while pulsatility characteristics are otherwise similar between lean and obese subjects.
- In congenital leptin deficiency (leptin or leptin receptor mutations), subjects present with hypogonadotropic hypogonadism, low FSH/LH, loss of LH pulsatility, lack of pubertal growth spurt, primary/secondary amenorrhea, growth delay with low IGF-I and IGF-BP3, and hypothalamic hypothyroidism; leptin administration in replacement doses restores these neuroendocrine features and immune function.
- In relative leptin deficiency (hypothalamic amenorrhea, lipoatrophy, anorexia nervosa), r-metHuLeptin in replacement doses restored reproductive function, induced ovulation, increased thyroxine, IGF-I, IGF-BP3, and bone markers, restored GnRH pulsatility, and improved insulin resistance and metabolic profile in HAART-induced lipoatrophy.
- In leptin-sufficient obese subjects with type 2 diabetes, r-metHuLeptin for 4 or 16 wk produced high pharmacologic leptin concentrations but did not activate the TNF-α system or raise cytokines/inflammatory markers above normal, supporting a permissive (not etiopathogenic) role for leptin in immune regulation; placebo-controlled trials in obese persons over 24 wk showed statistically significant but clinically unimpressive weight loss.
Methods
- Narrative review summarizing observational and interventional human studies on leptin physiology and pathophysiology, including pharmacokinetic studies and leptin replacement therapy.
- Evidence drawn from subjects with congenital complete leptin deficiency, leptin receptor mutations, lipoatrophy (congenital/acquired, including HIV/HAART-associated), hypothalamic amenorrhea, anorexia nervosa, and garden-variety obesity, plus healthy normal-weight subjects undergoing fasting/starvation with r-metHuLeptin administration.
- Includes two summary tables: factors regulating circulating leptin concentrations (Table 1) and leptin deficiency/resistance states with estimated prevalences (Table 2), plus a schematic figure of energy deficiency/excess effects on neuroendocrine axes.
Limitations
- Stated: the exact long-term effect of leptin on the hypothalamic-pituitary-GH-IGF axis remains to be fully elucidated; whether resolution of insulin resistance in congenital leptin deficiency is a primary leptin effect or secondary to fat loss/redistribution remains to be clarified; mechanisms of leptin's effects on the thyroid axis are not completely understood; more long-term interventional studies are needed in congenital leptin deficiency; whether r-metHuLeptin alone or combined with other treatments will find a therapeutic place remains to be seen.
- Stated: the role of leptin in the adrenal axis in humans remains controversial, with interventional studies in healthy normal-weight subjects failing to show an effect on adrenal steroids.
- Evident from the text: this is a narrative review without systematic search or meta-analytic synthesis, and several cited findings rest on small proof-of-concept studies; the authors also note their own laboratory received funds from Amgen and Amylin.
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Claims the paper makes
33 Not checked yet · 10 No basis given · 4 Own interpretation
None of the sources cited for this claim have been checked yet.
In the paper
“Leptin concentrations are positively correlated with the amount of body fat (4-10).”
§ Leptin in humans: lessons from translational research 1-4 > LEPTIN: THE PROTOTYPE ADIPOKINE
What the sources say
- Not checked yetcites [4] Brennan, 2007, Leptin and adiponectin: their role in diabetes., Curr Diab Rep source
- Not checked yetcites [5] Blüher, 2007, Leptin in reproduction., Curr Opin Endocrinol Diabetes Obes source
- Not checked yetcites [6] Brennan, 2006, Drug insight: the role of leptin in human physiology and pathophysiology: emerging clinical applications in leptin deficient states., Nat Clin Pract Endocrinol Metab source
- Not checked yetcites [7] Chan, 2006, Differential regulation of metabolic, neuroendocrine, and immune function by leptin in humans., Proc Natl Acad Sci USA source
- Not checked yetcites [8] Kelesidis, 2006, The emerging role of leptin in humans., Pediatr Endocrinol Rev
- Not checked yetcites [9] Chan, 2005, Role of leptin in energy-deprivation states: normal human physiology and clinical implications for hypothalamic amenorrhoea and anorexia nervosa., Lancet source
- Not checked yetcites [10] Lee, 2006, Recombinant methionyl human leptin therapy in replacement doses improves insulin resistance and metabolic profile in patients with lipoatrophy and metabolic syndrome induced by the highly active antiretroviral therapy., J Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“However, although obese subjects are hyperleptinemic compared with lean persons (11), they appear either to be tolerant or resistant to the central hypothalamic effects of leptin.”
§ Leptin in humans: lessons from translational research 1-4 > LEPTIN: THE PROTOTYPE ADIPOKINE
What the sources say
- Not checked yetcites [11] Kiess, 2008, Adipocytes and adipose tissue., Best Pract Res Clin Endocrinol Metab source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Children with congenital leptin deficiency are prone to early death as a result of severe infections during childhood because of defects in T cell number and function (28).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [28] Ozata, 1999, J Clin Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It also improved lipidemia and insulin resistance in HIVpositive patients with partial lipoatrophy (10,(22)(23)(24)(25)(26).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN GLUCOSE AND FAT METABOLISM OR DEVELOPMENT OF INSULIN RESISTANCE IN STATES OF LEPTIN DEFICIENCY
What the sources say
- Not checked yetcites [10] Lee, 2006, Recombinant methionyl human leptin therapy in replacement doses improves insulin resistance and metabolic profile in patients with lipoatrophy and metabolic syndrome induced by the highly active antiretroviral therapy., J Clin Endocrinol Metab source
- Not checked yetcites (22)(23)(24)(25)(26)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These disturbances can be completely reversed by leptin administration (6).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN GLUCOSE AND FAT METABOLISM OR DEVELOPMENT OF INSULIN RESISTANCE IN STATES OF LEPTIN DEFICIENCY
What the sources say
- Not checked yetcites [6] Brennan, 2006, Drug insight: the role of leptin in human physiology and pathophysiology: emerging clinical applications in leptin deficient states., Nat Clin Pract Endocrinol Metab source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The clinical features of hypothalamic hypogonadism and associated disturbances can be restored by leptin administration in replacement doses (17).”
§ Leptin in humans: lessons from translational research 1-4 > Leptin and the reproductive axis
What the sources say
- Not checked yetcites [17] Welt, 2004, Recombinant human leptin in women with hypothalamic amenorrhea., N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast to findings in rodents, subjects with mutations of the leptin gene or the leptin receptor gene present with normal adrenal function (16,18).”
§ Leptin in humans: lessons from translational research 1-4 > Leptin and the adrenal axis
What the sources say
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“However, immune function could be markedly improved with leptin replacement (29,30).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [29] Farooqi, 2002, Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency., J Clin Invest source
- Not checked yetcites [30] Farooqi, 2008, Monogenic human obesity., Front Horm Res
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It has been shown that leptin administration in replacement doses significantly improved glycemia, dyslipidemia, and hepatic steatosis in lipoatrophic, hypoleptinemic patients with severe insulin resistance.”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN GLUCOSE AND FAT METABOLISM OR DEVELOPMENT OF INSULIN RESISTANCE IN STATES OF LEPTIN DEFICIENCY
What the sources say
- Not checked yetcites [10] Lee, 2006, Recombinant methionyl human leptin therapy in replacement doses improves insulin resistance and metabolic profile in patients with lipoatrophy and metabolic syndrome induced by the highly active antiretroviral therapy., J Clin Endocrinol Metab source
- Not checked yetcites (22)(23)(24)(25)(26)
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In the paper
“We have not found direct supporting evidence of this hypothesis in our interventional studies (22).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN STATES OF LEPTIN EXCESS
What the sources say
- Not checked yetcites [22] Chan, 2005, Recombinant methionyl human leptin administration to achieve high physiologic or pharmacologic leptin levels does not alter circulating inflammatory marker levels in humans with leptin sufficiency or excess., J 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. 15
- Probably not a substantial claim. 1
In the paper
“Subjects with congenital leptin deficiency or loss of leptin function because of leptin mutations or leptin receptor mutations have clinically evident hypogonadotropic hypogonadism and present with low concentrations of follicle-stimulating hormone and luteinizing hormone and complete loss of luteinizing hormone pulsatility, lack of pubertal growth spurt, reduced expression of secondary sexual”
§ Leptin in humans: lessons from translational research 1-4 > Leptin and the reproductive axis
What the sources say
- Not checked yetcites [16] Farooqi, 2007, Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor., N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Leptin administration in replacement doses to healthy lean men during a 3-d starvation period significantly blunted the fasting-induced decrease in TSH pulsatility and increased free thyroxine to concentrations within 992S the normal range (19).”
§ Leptin in humans: lessons from translational research 1-4 > Leptin and the hypothalamic-pituitary-thyroid axis
What the sources say
- Not checked yetcites [19] Chan, 2003, The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men., J Clin Invest source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Administering leptin in replacement doses to healthy, normal-weight men after a period of acute fasting that resulted in low IGF-I concentrations partially prevented the decrease in IGF-I and IGF-BP3 but had no (short-term) effect on circulating concentrations of GH (19).”
§ Leptin in humans: lessons from translational research 1-4 > Leptin and the hypothalamic-pituitary-growth hormoneinsulin-like growth factor I axis
What the sources say
- Not checked yetcites [19] Chan, 2003, The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men., J Clin Invest source
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
“These leptindeficient subjects respond in a dramatic fashion to leptin administered in replacement doses, which induces markedly decreased appetite and food intake and which in turn result in a significant reduction in body weight (28)(29)(30).”
§ Leptin in humans: lessons from translational research 1-4 > Leptin replacement therapy in complete leptin deficiency
What the sources say
- Not checked yetcites [28] Ozata, 1999, J Clin Endocrinol Metab source
- Not checked yetcites [29] Farooqi, 2002, Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency., J Clin Invest source
- Not checked yetcites [30] Farooqi, 2008, Monogenic human obesity., Front Horm Res
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
“Interventional studies in women with hypothalamic amenorrhea and low circulating leptin concentrations have proven the concept that r-metHuLeptin in replacement doses may restore reproductive function, induce ovulation, and increase circulating concentrations of thyroxine, IGF-I, IGF-BP3, bone alkaline phosphatase, and other bone markers.”
§ Leptin in humans: lessons from translational research 1-4 > Leptin replacement therapy in relative leptin deficiency
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“The result is not only an increasing degree of obesity associated with increased lipid storage in muscle, liver, and other tissues but also dysfunction of several neuroendocrine axes, including the reproductive, thyroid, and adrenal axes, as well as abnormal function of the immune and autonomic system (ie, thermoregulation, energy expenditure, and others) (5, 13, 14).”
§ Leptin in humans: lessons from translational research 1-4 > LEPTIN: THE PROTOTYPE ADIPOKINE
What the sources say
- Not checked yetcites [5] Blüher, 2007, Leptin in reproduction., Curr Opin Endocrinol Diabetes Obes source
- Not checked yetcites [13] Myers, 2008, Mechanisms of leptin action and leptin resistance., Annu Rev Physiol source
- Not checked yetcites [14] Blüher S, Mantzoros CS. Insulin resistance in states of energy excess–pathophysiological concepts. In: Mantzoros CS, ed. The metabolic syndrome.Totowa, NJ: Humana Press, in press.
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“These findings are consistent with physiology studies, which have proven that leptin is a crucial hormonal factor for regulating several physiologic processes, including inflammation, angiogenesis, hematopoiesis, immune function, and reproduction.”
§ Leptin in humans: lessons from translational research 1-4 > LEPTIN: THE PROTOTYPE ADIPOKINE
boosteddirect- Asserted: passes — The authors put it forward as true.
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It 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
“In contrast, states of energy excess such as garden-variety obesity are associated with hyperleptinemia that reflects either leptin tolerance or leptin resistance.”
- Also stated in: § ROLE OF LEPTIN IN STATES OF LEPTIN EXCESS · hedged
“Obesity is associated with hyperleptinemia, which may reflect either leptin tolerance or leptin resistance.”
§ Leptin in humans: lessons from translational research 1-4 > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Also stated in: § ROLE OF LEPTIN IN STATES OF LEPTIN EXCESS · hedged
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
“As shown by animal studies as well as observational studies in humans with congential leptin deficiency or obesity-related hyperleptinemia, both leptin excess and states of energy deprivation associated with leptin deficiency may increase the individual susceptibility to infection”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Leptin has been shown to have several effects on the innate immune system in leptin-deficient states: It exerts direct effects on macrophages by up-regulating the phagocytic activity, stimulates the secretion of proinflammatory cytokines, and stimulates chemotaxis in polymorphonuclear cells (6).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [6] Brennan, 2006, Drug insight: the role of leptin in human physiology and pathophysiology: emerging clinical applications in leptin deficient states., Nat Clin Pract Endocrinol Metab source
boosteddirect- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“Thus, leptin may increase circulating cytokine concentrations and regulate the T helper type 1 and 2 cell immune balance in states of congenital leptin deficiency and immune dysfunction, supporting a role for leptin in regulating immune function in these conditions (29,30).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [29] Farooqi, 2002, Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency., J Clin Invest source
- Not checked yetcites [30] Farooqi, 2008, Monogenic human obesity., Front Horm Res
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.
None of the sources cited for this claim have been checked yet.
In the paper
“Interventional studies investigating the effect of leptin administration to persons with leptin deficiency compared with leptin sufficiency or leptin excess could clearly show a role for leptin in regulating the immune system in states of leptin deficiency, but not leptin excess, as seen in obesity (22,27,31).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [22] Chan, 2005, Recombinant methionyl human leptin administration to achieve high physiologic or pharmacologic leptin levels does not alter circulating inflammatory marker levels in humans with leptin sufficiency or excess., J Clin Endocrinol Metab source
- Not checked yetcites [27] Matarese, 2007, Leptin and adipocytokines: bridging the gap between immunity and atherosclerosis., Curr Pharm Des source
- Not checked yetcites [31] Chan, 2005, J Clin Endocrinol Metab source
boosteddirect- Asserted: passes — The authors put it forward as true.
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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
“Very rare genetic forms of obesity result from congenital leptin deficiency as a result of mutations in the leptin genes, which are frequently associated with consanguineous marriage.”
§ Leptin in humans: lessons from translational research 1-4 > Leptin replacement therapy in complete leptin deficiency
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
“These data support a permissive role for leptin in the regulation of the immune system but do not support an etiopathogenic role for leptin in proinflammatory states associated with leptin excess such as obesity (32).”
§ Leptin in humans: lessons from translational research 1-4 > ROLE OF LEPTIN IN THE REGULATION OF IMMUNE FUNCTION
What the sources say
- Not checked yetcites [32] Brennan, 2007, Circulating leptin levels are not associated with cardiovascular morbidity and mortality in women with diabetes: a prospective cohort study., Diabetologia source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Subsequent studies have also shown that leptin is involved in regulating several neuroendocrine axes, immune function, and glucose and lipid metabolism.”
§ Leptin in humans: lessons from translational research 1-4 > SUMMARY AND FURTHER DIRECTIONS
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“Relative leptin deficiency, such as occurs in congenital or acquired lipodystrophies, thin, very athletic women with hypothalamic amenorrhea, and anorexia nervosa, does respond to leptin administration 152 153.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [152]
Citations
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Research works printed but not linked: 1
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Cited by
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Adipose Tissue as an Endocrine Organ
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Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome
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Metadata
- Authors
- Blüher, S., & Mantzoros, C. S.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Mantzoros, Christos S
- Venue
- The American Journal of Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 2009-03
- Volume
- 89
- Issue
- 3
- Pages
- 991S-997S
- ISSN
- 0002-9165 (ISSN-L)
- PMC
- PMC2667664
- OpenAlex
- W2085745363
- Semantic Scholar
- 754cc7437a42584ee480fe9f8c45e1cc97089c03
- Cited by
- 203
- References
- 43
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 11 · 2022: 8 · 2021: 12 · 2020: 7 · 2019: 7 · 2018: 3 · 2017: 5 · 2016: 14 · 2015: 19 · 2014: 14 · 2013: 12 · 2012: 27
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Nutrition (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK079929, DK 79929, DK 58785)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin, leptin deficiency, leptin replacement therapy, congenital leptin deficiency, hypothalamic amenorrhea, anorexia nervosa, lipodystrophy, insulin resistance, leptin resistance, obesity, hyperleptinemia, energy balance, food intake regulation, energy expenditure, immune function, glucose metabolism, fat metabolism, neuroendocrine dysfunction
- MeSH terms
- Animals, Humans, Neurosecretory Systems, Leptin
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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