Effects of leptin replacement on macro- and micronutrient preferences

Licinio, Júlio; Ribeiro, Luciana; Busnello, João Vicente; Delibaşı, Tuncay; Thakur, Sarika; Elashoff, Robert M.; Sharma, A. M.; Jardack, Patricia; DePaoli, Alex M.; Wong, Ma-Li

doi:10.1038/sj.ijo.0803703

Cited by 18 publications

(8 citation statements)

References 6 publications

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“…The other study investigated the effects of leptin replacement on the macro- and micronutrient preferences in leptin-deficient adults. After leptin replacement, all the patients initially presented a marked reduction in the intake of macro- and micro-nutrients, and their mean daily caloric intake dropped to 50% with a shift toward a higher percentage consumption of fats and a decrease in the intake of carbohydrates (Licinio et al, 2007b). The other patients were studied while off and on leptin therapy at a stable body weight, and significant differences were measured in their levels of macronutrients, vitamins, and minerals (Licinio et al, 2007a).…”

Section: Clinical Trial Of Leptin Replacement Therapymentioning

confidence: 99%

The role of leptin in the control of insulin-glucose axis

et al. 2013

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Obesity and diabetes mellitus are great public health concerns throughout the world because of their increasing incidence and prevalence. Leptin, the adipocyte hormone, is well known for its role in the regulation of food intake and energy expenditure. In addition to the regulation of appetite and satiety that recently has attracted much attentions, insight has also been gained into the critical role of leptin in the control of the insulin-glucose axis, peripheral glucose and insulin responsiveness. Since the discovery of leptin, leptin has been taken for its therapeutic potential to obesity and diabetes. Recently, the therapeutic effects of central leptin gene therapy have been reported in insulin-deficient diabetes in obesity animal models such as ob/ob mise, diet-induced obese mice, and insulin-deficient type 1 diabetes mice, and also in patients with inactivating mutations in the leptin gene. Herein, we review the role of leptin in regulating feeding behavior and glucose metabolism and also the therapeutic potential of leptin in obesity and diabetes mellitus.

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Section: Clinical Trial Of Leptin Replacement Therapymentioning

confidence: 99%

The role of leptin in the control of insulin-glucose axis

et al. 2013

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“…In the adults, leptin replacement decreased energy intake from 2,384 ± 946 kcal/day to 1,179 ± 790 kcal/day (Figure 4). In addition, leptin replacement changed the macronutrient content of the patients’ diet, with an increase in carbohydrate and a decrease in fat consumption (20). In the child, after two years, caloric in-take decreased from 2,709 ± 370 to 2,194 ± 292 kcal/ day, which is 106% of the recommended caloric intake for a boy this age, height and weight (14).…”

Section: Phenotype Before and During Treatmentmentioning

confidence: 99%

Congenital leptin deficiency: diagnosis and effects of leptin replacement therapy

Paz-Filho

Mastronardi

Delibaşı

et al. 2010

Arq Bras Endocrinol Metab

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SUMMARY To describe our 10-year experience in treating leptin-deficient humans. Three adults and one boy presented with childhood-onset morbid obesity, hypogonadism and family history of obesity and early death. Serum leptin was inappropriately low. A recessive C105T leptin gene mutation was identified. Metabolic and endocrine assessments were conducted, before and while on and off leptin. The adults’ body mass index decreased from 51.2 ± 2.5 to 29.5 ± 2.8 kg/m2. Serum lipids normalized, insulin resistance decreased, and one of the initially diabetic females became normoglycemic. Hypogonadotropic hypogonadism was reversed, and other changes were observed in the adrenal, sympathetic, somatotropic and thyroid functions. Leptin replacement therapy reverses endocrine and metabolic alterations associated with leptin deficiency. Some of these results may be extrapolated to other diseases.

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“…This simple but attractive concept has been gradually replaced by more elaborate neuroanatomical models, which have incorporated the concept of the distributed nature of the neuronal networks that control food intake (67). Leptin can modulate several different aspects of feeding behavior, including meal size (68,69), food reward (70,71), and food preference (72,73). Collectively, these observations suggest that the neural circuits underlying leptin actions on food intake are highly complex.…”

Section: Figurementioning

confidence: 99%

Sixteen years and counting: an update on leptin in energy balance

Gautron¹,

Elmquist²

2011

J. Clin. Invest.

311

251

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Cloned in 1994, the ob gene encodes the protein hormone leptin, which is produced and secreted by white adipose tissue. Since its discovery, leptin has been found to have profound effects on behavior, metabolic rate, endocrine axes, and glucose fluxes. Leptin deficiency in mice and humans causes morbid obesity, diabetes, and various neuroendocrine anomalies, and replacement leads to decreased food intake, normalized glucose homeostasis, and increased energy expenditure. Here, we provide an update on the most current understanding of leptin-sensitive neural pathways in terms of both anatomical organization and physiological roles. IntroductionThe nervous system regulates energy balance at the organismal level by constantly adjusting energy intake, expenditure, and storage. The influence of the nervous system over metabolic functions was first suggested at the beginning of the 20th century when excessive adiposity was associated with pituitary tumors and injury to the hypothalamus (1). However, it was not until the 1940s that selective surgical lesions of certain hypothalamic areas were found to result in extreme obesity or leanness in rats (2, 3). Over the last few decades, numerous discoveries substantially extended our understanding of the neural control of metabolism. However, it is safe to say that none were more important than the cloning of the ob gene by Friedman and colleagues in 1994 (4). The ob gene encodes the protein leptin, which is a hormone produced and secreted by the white adipose tissue, and consequently, its circulating levels are closely related to body fat mass (5, 6). Leptin deficiency in mice homozygous for a mutant ob gene (ob/ob mice) causes morbid obesity, diabetes, and various neuroendocrine anomalies, and leptin replacement leads to decreased food intake, normalized glucose homeostasis, and increased energy expenditure (7-10). Several splice variants of the leptin receptor have been identified, and the "short forms" are widely expressed in multiple tissues (11). The "long form" of the leptin receptor encodes a protein with a longer cytoplasmic domain (OB-Rb) that is highly expressed in particular sites within the CNS (refs. 10, 12, and Table 1). The short forms of the leptin receptor are also present within the CNS (11), but OB-Rb is sufficient for leptin actions on metabolism (13,14). OB-Rb is a type 1 cytokine receptor, which stimulates the JAK/STAT3 pathway (15) and PI3K (16,17). Leptin induces transcriptional changes of several genes via the JAK/STAT3 pathway, and rapid changes in cellular activity and membrane potential may underlie the acute actions of leptin (18). While actions of this hormone in peripheral tissues have been identified, studies in genetically modified mice have demonstrated that leptin action only in the CNS is sufficient to regulate body weight, feeding, energy expenditure, and glucose metabolism (13,(19)(20)(21).Since leptin is clearly not the only metabolic signal acting on the brain, the range of its effects on behavior, metabolism, and endocrinology is trul...

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Effects of leptin replacement on macro- and micronutrient preferences

Cited by 18 publications

References 6 publications

The role of leptin in the control of insulin-glucose axis

The role of leptin in the control of insulin-glucose axis

Congenital leptin deficiency: diagnosis and effects of leptin replacement therapy

Sixteen years and counting: an update on leptin in energy balance

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