Adipokine levels in Cushing's syndrome; elevated resistin levels in female patients with Cushing's syndrome

Kršek, Michal; Silha, Josef V.; Ježková, J; Hána, Václav; Jakóbisiak, Marek; Weiss, V; Štěpán, J; Murphy, Liam

doi:10.1111/j.1365-2265.2003.01987.x

Cited by 44 publications

(53 citation statements)

References 51 publications

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“…Resistin is significantly higher in female CS patients than in female control subjects and does not significantly change after cure, despite improvement of obesity and metabolic profile (116). TNFa levels are unchanged in CS (115).…”

Section: European Journal Of Endocrinologymentioning

confidence: 85%

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Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

144

121

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Cushing's syndrome (CS) patients have increased mortality primarily due to cardiovascular events induced by glucocorticoid (GC) excess-related severe metabolic changes. Glucose metabolism abnormalities are common in CS due to increased gluconeogenesis, disruption of insulin signalling with reduced glucose uptake and disposal of glucose and altered insulin secretion, consequent to the combination of GCs effects on liver, muscle, adipose tissue and pancreas. Dyslipidaemia is a frequent feature in CS as a result of GC-induced increased lipolysis, lipid mobilisation, liponeogenesis and adipogenesis. Protein metabolism is severely affected by GC excess via complex direct and indirect stimulation of protein breakdown and inhibition of protein synthesis, which can lead to muscle loss. CS patients show changes in body composition, with fat redistribution resulting in accumulation of central adipose tissue. Metabolic changes, altered adipokine release, GC-induced heart and vasculature abnormalities, hypertension and atherosclerosis contribute to the increased cardiovascular morbidity and mortality. In paediatric CS patients, the interplay between GC and the GH/IGF1 axis affects growth and body composition, while in adults it further contributes to the metabolic derangement. GC excess has a myriad of deleterious effects and here we attempt to summarise the metabolic comorbidities related to CS and their management in the perspective of reducing the cardiovascular risk and mortality overall.

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Section: European Journal Of Endocrinologymentioning

confidence: 85%

“…Leptin does not seem to be acutely affected by the cortisol drop following neurosurgery but it has been found to be decreased in patients after long-term remission (116).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

144

121

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“…In human medicine, a study found that patients with Cushing's syndrome had lower adiponectin levels than the controls, which suggests that hypercortisolemia directly affected the adiponectin levels independent of body weight 43. However, another study reported that the serum adiponectin levels in patients with Cushing's syndrome did not differ from those in the control group and they were not changed significantly after hypophysectomy, despite a significant decrease in the body fat mass, insulin resistance, and cortisol 36, 44. In veterinary medicine, a recent study showed that the circulating adiponectin concentrations in 20 PDH dogs with blindness were significantly lower than those of 20 healthy dogs 18.…”

Section: Discussionmentioning

confidence: 99%

“…This might be attributable to the persistence of hypercortisolemia for parts of each day, and to persistently higher visceral fat mass after the treatment. In human studies, subjects with Cushing's syndrome have persistent central fat mass, higher leptin concentrations, and other abnormal adipokines, even after long‐term cure 35, 36. Therefore, it is possible that the maintenance of hyperleptinemia might have been the result of secretion of leptin by the persistent central fat mass in dogs with PDH.…”

Section: Discussionmentioning

confidence: 99%

Serum Adipokine Concentrations in Dogs with Naturally Occurring Pituitary‐Dependent Hyperadrenocorticism

Cho

Paek

Kang

et al. 2013

Veterinary Internal Medicne

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BackgroundAn excess of intra‐abdominal fat is observed frequently in dogs with hyperadrenocorticism (HAC). Adipokine dysregulation is a possible cause of complications related to visceral obesity, but little information is available on adipokine in dogs with naturally occurring HAC.ObjectivesTo examine the differences in the circulating adipokines concentrations in overweight dogs with and without pituitary‐dependent HAC (PDH).AnimalsThirty healthy dogs and 15 client‐owned dogs with PDH.MethodsCase–controlled observational study, which enrolled 15 overweight dogs diagnosed with PDH and 30 otherwise healthy dogs of similar body condition score. Nine of 15 dogs with PDH were treated with low‐dose trilostane twice daily and reassessed after treatment.ResultsThe serum leptin (P < .0001) and insulin (P < .0001) concentrations were significantly higher in the PDH group (leptin, 22.8 ± 8.8 [mean ± SD]; insulin, 9.1 ± 6.1) than the healthy group (leptin, 4.9 ± 3.7; insulin, 1.9 ± 0.9). However, there were no significant differences in the adiponectin, resistin, tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6, IL‐10, and IL‐18 levels between the 2 groups. In the PDH group, the serum cortisol concentrations had a linear association with the leptin concentrations, and there were significant decreases in the leptin (P = .0039) and insulin (P = .0039) levels after trilostane treatment. However, the leptin and insulin levels remained higher after trilostane treatment than in healthy control dogs with similar body condition score.Conclusions and Clinical ImportanceHypercortisolemia in dogs with PDH might upregulate the circulating leptin levels. However, a large population‐based study will be necessary to determine whether the upregulation of leptin is involved directly with the complications caused by HAC.

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“…Since visceral adipose tissue is considered to be the major source of adipokines, the increase in visceral fat mass with the resultant increase in plasma adipokine levels may at least partly be responsible for the occurrence of insulin resistance in cushing syndrome with glucocorticoid excess. indeed, glucocorticoid is shown to stimulate the release of resistin from mouse adipocytes [10], and serum resistin levels are elevated in cushing syndrome [11], indicating that resistin may be involved in the glucocorticoid-induced insulin resistance.…”

Section: Evaluation Of Metabolic Parameters In Crh-tg Micementioning

confidence: 99%

Plasma Adiponectin Levels are Increased Despite Insulin Resistance in Corticotropin-releasing Hormone Transgenic Mice, an Animal Model of Cushing Syndrome

et al. 2009

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Abstract. adiponectin (adN), an adipokine derived from the adipose tissue, has an insulin-sensitizing effect, and plasma adN is shown to be decreased in obesity and/or insulin resistant state. to clarify whether changes in adN are also responsible for the development of glucocorticoid-induced insulin resistance, we examined adN concentration in plasma and adN expression in the adipose tissue, using corticotropin-releasing hormone (cRH) transgenic mouse (cRH-tg), an animal model of cushing syndrome. We found, unexpectedly, that plasma adN levels in cRHTg were significantly higher than those in wild-type littermates (wild-type: 19.7±2.5, CRH-Tg: 32.4±3.1µg/mL, p<0.01). On the other hand, AdN mRNA and protein levels were significantly decreased in the adipose tissue of cRH-tg. Bilateral adrenalectomy in cRH-tg eliminated both their cushing's phenotype and their increase in plasma AdN levels (wild-type/sham: 9.4±0.5, CRH-Tg/sham: 15.7±2.0, CRH-Tg/ADX: 8.5±0.4µg/mL). These results strongly suggest that adN is not a major factor responsible for the development of insulin resistance in cushing syndrome. our data also suggest that glucocorticoid increases plasma adN levels but decreases adN expression in adipocytes, the latter being explained possibly by the decrease in adN metabolism in the cushing state.

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Adipokine levels in Cushing's syndrome; elevated resistin levels in female patients with Cushing's syndrome

Abstract: Here we report for the first time that resistin levels are significantly elevated in CS patients and may be important in the insulin resistance associated with glucocorticoid excess.

Cited by 44 publications

References 51 publications

Metabolic comorbidities in Cushing's syndrome

Metabolic comorbidities in Cushing's syndrome

Serum Adipokine Concentrations in Dogs with Naturally Occurring Pituitary‐Dependent Hyperadrenocorticism

Plasma Adiponectin Levels are Increased Despite Insulin Resistance in Corticotropin-releasing Hormone Transgenic Mice, an Animal Model of Cushing Syndrome

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