In VitroLipolytic Effect of Leptin on Mouse Adipocytes: Evidence for a Possible Autocrine/Paracrine Role of Leptin

Frühbeck, Gema; Aguado, Miriam; Ja, Martínez

doi:10.1006/bbrc.1997.7716

Cited by 248 publications

(165 citation statements)

References 25 publications

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“…12 Leptin can exert its effect as an autocrine or paracrine signal modulating the rate of synthesis and degradation of lipids. 29,30 Because adipose tissue is a key organ involved in energy handling and storage, changes at the level of the leptin receptor in adipose tissue can be of great importance in the development of obesity and its related metabolic disorders. In fact, a lower mRNA abundance of OB-Rb in the adipose tissue has been described in humans with morbid obesity 31 and we have previously described that chronic HF-diet feeding results in lower expression levels of OB-Rb in WAT in male but not in female rats.…”

Section: Discussionmentioning

confidence: 99%

Leptin intake during the suckling period improves the metabolic response of adipose tissue to a high-fat diet

2010

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Background: The intake of leptin during the suckling period protects against obesity and improves insulin and central leptin sensitivity in adult rats. Objective: We analyzed whether leptin treatment to neonates may also improve later peripheral leptin sensitivity in adipose tissue under high-fat (HF) diet conditions. Design: Male rats were supplemented with a daily oral dose of leptin or the vehicle (controls) during the suckling period. After weaning, animals were fed a normal-fat or an HF diet until the age of 6 months. At this age, mRNA and protein levels of the longform leptin receptor (OB-Rb) and the expression of other genes related with energy metabolism were measured in various adipose depots (inguinal, mesenteric and retroperitoneal). Results: HF-diet feeding resulted in lower OB-Rb mRNA and protein levels in internal depots in controls but not in leptin-treated animals; these animals maintained OB-Rb mRNA and protein levels under HF-diet conditions in these depots, particularly in the mesenteric one, and this was accompanied by increased expression of genes related with energy uptake (GLUT4, CD36), fatty acid oxidation (peroxisome proliferator activated receptor-a (PPARa), CPT1, UCP3) and lipogenesis (PPARg, GPAT). Leptintreatment also ameliorated HF-diet-induced hepatic fat accumulation occurring in control animals. Conclusion: Leptin treatment during the suckling period may improve the lasting effects of HF-diet feeding on leptin receptor abundance in the adipose tissue and increase its oxidative capacity, resulting in a better handling and partitioning of excess fuel. This, together with the described improvement of central leptin sensitivity, may explain why these animals are more protected against diet-induced obesity and its metabolic-related disorders.

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Section: Discussionmentioning

confidence: 99%

Leptin intake during the suckling period improves the metabolic response of adipose tissue to a high-fat diet

2010

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“…The two opposing biochemical processes, lipolysis and lipid synthesis, are controlled by different enzymes, which are differentially regulated by hormones. Leptin can act as an autocrine or paracrine signal to change the rate of synthesis and degradation of lipids [6,22]. Therefore, changes at the level of the leptin receptor in the adipose tissue can be of great importance in the development of obesity and other metabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

Effect of high-fat diet feeding on leptin receptor expression in white adipose tissue in rats: depot- and sex-related differential response

2009

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Previous studies have illustrated the importance of leptin receptor (OB-Rb) mediated action on adipocytes in the regulation of body weight. The aim of the present study was to investigate in male and female rats the effects of high-fat (HF) diet feeding on the expression levels of OB-Rb in different depots of white adipose tissue (WAT), and its relation to fatty acid oxidation capacity. Male and female Wistar rats were fed until the age of 6 months with a normal-fat (NF) or non-isocaloric HF-diet (10 and 45% calories from fat, respectively). At this age, the weight of three different fat depots (retroperitoneal, mesenteric and inguinal) and the expression levels of OB-Rb, PPARa and CPT1 in these depots were measured. HF-diet feeding resulted in an increase in the weight of the different fat depots, the retroperitoneal depot being the one with the greatest increase in both sexes. In this depot, HF-diet feeding resulted in a significant decrease in OB-Rb mRNA levels, more marked in male than in female rats. In the mesenteric depot, the effects of HF-diet feeding on OB-Rb mRNA levels were sex-dependent: they decreased in males rats (associated with a decrease in PPARa and CPT1 mRNA levels), but increased in female rats. In the inguinal depot, OB-Rb expression was not affected by HF-diet feeding. These results show that a chronic intake of an HF-diet altered the expression of OB-Rb in WAT in a depot and sex-dependent manner. The decreased expression of OB-Rb in the internal depots of male rats under HF-diet feeding, with the resulting decrease in leptin sensitivity, can help to explain the higher tendency of males to suffer from obesity-linked disorders under HF-diet conditions.

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“…In addition, leptin treatment for 24 h increases LPL mRNA in primary cultures of brown adipocytes [66]. The presence of OB-Rb in white and brown adipose tissues has been substantiated by the detection of its transcripts by RT-PCR and leptin treatment in vivo and in vitro activating the Jak/STAT pathway [67]. These effects of leptin are prevented in fa/fa rats with leptin receptor mutation, suggesting that leptin receptor signalling directly contributes to the effect of leptin [67].…”

Section: Effects Of Leptin On Glucose and Fat Metabolismmentioning

confidence: 94%

New insights into sympathetic regulation of glucose and fat metabolism

2000

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Since the observation by Claude Bernard in the 1850 s that puncture of the floor of the fourth ventricle in dogs results in the appearance of transient glucosuria, the central nervous system (CNS) has been implicated in the control of certain metabolic processes of energy homeostasis mainly through neuroendocrine systems. After its recent discovery, leptin, an adipocyte hormone, has been proposed to signal the CNS to modulate autonomic outflow and food intake, leading to alterations of energy metabolism [1,2]. Leptin has been suggested to increase sympathetic outflow and disturbances of leptin signalling lead to Diabetologia (2000) 43: 533±549 ReviewsNew insights into sympathetic regulation of glucose and fat metabolism AbstractThe autonomic nervous system modulates glucose and fat metabolism through both direct neural effects and hormonal effects. This review presents recent concepts on the sympathetic regulation of glucose and fat metabolism. Focally released norepinephrine from sympathetic nerves is likely to increase glucose uptake in skeletal muscle and adipose tissues independent of insulin but norepinephrine does not contribute so much as epinephrine to hepatic glucose production. Epinephrine increases hepatic glucose production and inhibits insulin secretion and the glucose uptake by tissues that is induced by insulin. Additionally, catecholamines can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. It is likely that b-(b3)-adrenergic receptors mediate these responses. Alterations of central neurotransmission and environmental factors can change the relative contribution of sympathetic outflow to the pancreas, liver, adrenal medulla and adipose tissues, leading to the modulation of glucose and fat metabolism. Recent studies have proposed that leptin, an adipocyte hormone, affects the central nervous system to increase sympathetic outflow independent of feeding. The effects of leptin on glucose and fat metabolism could be in part mediated by the sympathetic nervous system. Studies using mice with a genetic disruption of serotonin 5-HT2 c receptor indicate that central neural mechanisms in the regulation of sympathetic outflow and satiety could be dissociated. Abnormalities of sympathetic effects, including disturbances of leptin and b3-adrenergic receptor signalling, are likely to cause obesity and impaired glucose tolerance in rodents and humans. These findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus. [Diabetologia (2000) 43: 533±549]

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In VitroLipolytic Effect of Leptin on Mouse Adipocytes: Evidence for a Possible Autocrine/Paracrine Role of Leptin

Cited by 248 publications

References 25 publications

Leptin intake during the suckling period improves the metabolic response of adipose tissue to a high-fat diet

Leptin intake during the suckling period improves the metabolic response of adipose tissue to a high-fat diet

Effect of high-fat diet feeding on leptin receptor expression in white adipose tissue in rats: depot- and sex-related differential response

New insights into sympathetic regulation of glucose and fat metabolism

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