Serum Immunoreactive-Leptin Levels are Increased in Patients With Cushing's Syndrome

Leal‐Cerro, Alfonso; Rv, Considine; Peinó, R.; Venegas, Eva; Astorga, R.; Ff, Casanueva; Dieguez, C.

doi:10.1055/s-2007-979884

Cited by 93 publications

(56 citation statements)

References 5 publications

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“…However, there is no support either in experimental animals (Gualillo et al 1999) or in the present work, for a direct PRL action on the adipocyte production of leptin. Similarly, hypercorticoid states are associated with enhanced leptin levels (Leal-Cerro et al 1996, Masuzaki et al 1997 and glucocorticoids are potent inducers of leptin synthesis and secretion at the adipose tissue level (Considine et al 1997, Casabiell et al 1998, but no data link ACTH with a direct action on the adipocyte and the present results also discard that mechanism. Finally, while the action of leptin over gonadotrophin-releasing hormone secretion by the hypothalamus is well supported (Yu et al 1997, Carro et al 1999, Magni et al 1999, no direct interaction between LH or FSH and leptin has been reported previously or observed in this work.…”

Section: Discussioncontrasting

confidence: 64%

TSH stimulates leptin secretion by a direct effect on adipocytes

Menéndez

Baldelli²,

Camiña³

et al. 2003

Journal of Endocrinology

142

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Leptin is a circulating hormone secreted by adipose tissue which acts as a signal to the central nervous system where it regulates energy homeostasis and neuroendocrine processes. Although leptin modulates the secretion of several pituitary hormones, no information is available regarding a direct action of pituitary products on leptin release. However, it has been pointed out that leptin and TSH have a coordinated pulsatility in plasma. In order to test a direct action of TSH on in vitro leptin secretion, a systematic study of organ cultures of human omental adipose tissue was performed in samples obtained at surgery from 34 patients of both sexes during elective abdominal surgery. TSH powerfully stimulated leptin secretion by human adipose tissue in vitro. In contrast, prolactin, ACTH, FSH and LH were devoid of action. These results suggest that leptin and the thyroid axis maintain a complex and dual relationship and open the possibility that plasmatic changes in TSH may contribute to the regulation of leptin pulses.

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Section: Discussioncontrasting

confidence: 64%

TSH stimulates leptin secretion by a direct effect on adipocytes

Menéndez

Baldelli²,

Camiña³

et al. 2003

Journal of Endocrinology

142

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“…First, circulating leptin level is correlated with the body fat mass in dogs,21 so it is possible that an increased fat mass in the abdomen might lead to excessive hyperleptinemia. Second, in humans, it has been suggested that an increase in visceral fat has a relatively stronger effect on serum leptin in patients with Cushing's syndrome than it does in subjects with normal cortisolemia 22, 23, 24, 25. Therefore, it is also possible that an excess of endogenous cortisol promotes the production of leptin by adipose tissue without a change in fat mass 24.…”

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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“…60,61 This function is chie¯y accomplished by decreasing food consumption, 62,63 an effect probably mediated through inhibition of neuropeptide Y (NPY) secretion 64 ± 66 and enhancement of energy expenditure. 67,68 Indeed, serum leptin levels are elevated in simple obesity 69 and in clinical conditions associated with increased body fat such as Cushing's syndrome 70 and adult GH de®ciency, 71,72 and low in anorexia nervosa. 73,74 On the other side, GH also takes part in the regulation of body composition through a marked nitrogen sparing and lipolytic effect, 75 as shown by its administration to obese 76 and GH de®cient patients.…”

Section: Leptin As a Peripheral Signal For Gh Regulationmentioning

confidence: 99%

Growth hormone in obesity

1999

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Growth hormone (GH) secretion, either spontaneous or evoked by provocative stimuli, is markedly blunted in obesity. In fact obese patients display, compared to normal weight subjects, a reduced half-life, frequency of secretory episodes and daily production rate of the hormone. Furthermore, in these patients GH secretion is impaired in response to all traditional pharmacological stimuli acting at the hypothalamus (insulin-induced hypoglycaemia, arginine, galanin, L-dopa, clonidine, acute glucocorticoid administration) and to direct somatotrope stimulation by exogenous growth hormone releasing hormone (GHRH). Compounds thought to inhibit hypothalamic somatostatin (SRIH) release (pyridostigmine, arginine, galanin, atenolol) consistently improve, though do not normalize, the somatotropin response to GHRH in obesity. The synthetic growth hormone releasing peptides (GHRPs) GHRP-6 and hexarelin elicit in obese patients GH responses greater than those evoked by GHRH, but still lower than those observed in lean subjects. The combined administration of GHRH and GHRP-6 represents the most powerful GH releasing stimulus known in obesity, but once again it is less effective in these patients than in lean subjects. As for the peripheral limb of the GH ± insulin-like growth factor I (IGF-I) axis, high free IGF-I, low IGF-binding proteins 1 (IGFBP-1) and 2 (IGFBP-2), normal or high IGFBP-3 and increased GH binding protein (GHBP) circulating levels have been described in obesity. Recent evidence suggests that leptin, the product of adipocyte speci®c ob gene, exerts a stimulating effect on GH release in rodents; should the same hold true in man, the coexistence of high leptin and low GH serum levels in human obesity would ®t in well with the concept of a leptin resistance in this condition. Concerning the in¯uence of metabolic and nutritional factors, an impaired somatotropin response to hypoglycaemia and a failure of glucose load to inhibit spontaneous and stimulated GH release are well documented in obese patients; furthermore, drugs able to block lipolysis and thus to lower serum free fatty acids (NEFA) signi®cantly improve somatotropin secretion in obesity. Caloric restriction and weight loss are followed by the restoration of a normal spontaneous and stimulated GH release. On the whole, hypothalamic, pituitary and peripheral factors appear to be involved in the GH hyposecretion of obesity. A SRIH hypertone, a GHRH de®ciency or a functional failure of the somatotrope have been proposed as contributing factors. A lack of the putative endogenous ligand for GHRP receptors is another challenging hypothesis. On the peripheral side, the elevated plasma levels of NEFA and free IGF-I may play a major role. Whatever the cause, the defect of GH secretion in obesity appears to be of secondary, probably adaptive, nature since it is completely reversed by the normalization of body weight. In spite of this, treatment with biosynthetic GH has been shown to improve the body composition and the metabolic ef®cacy of lean body mass in obese pa...

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Serum Immunoreactive-Leptin Levels are Increased in Patients With Cushing's Syndrome

Cited by 93 publications

References 5 publications

TSH stimulates leptin secretion by a direct effect on adipocytes

TSH stimulates leptin secretion by a direct effect on adipocytes

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

Growth hormone in obesity

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