Developmental increases in plasma leptin binding activity and tissue Ob-Re mRNA expression in the rat

Smith, Jeremy Troy; Mark, Peter J.; Waddell, Brendan J.

doi:10.1677/joe.1.06045

Cited by 14 publications

(10 citation statements)

References 47 publications

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“…The implication of this for leptin signaling is not clear, however, because plasma concentration of the soluble leptin receptor-e, which acts as a plasma binding protein that reduces leptin signaling, also is much higher in postpubertal male rats than postpubertal female rats (681).…”

Section: R1237 Sex Differences In the Physiology Of Eatingmentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Section: R1237 Sex Differences In the Physiology Of Eatingmentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

View full text Add to dashboard Cite

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“…Oestradiol is known to enhance leptin synthesis and to induce leptin gene expression in subcutaneous, perirenal and parametrial rat adipocytes . Another potential mechanism explaining sex differences in leptin responsiveness is the relatively greater binding to the soluble form of the leptin receptor in males relative to females, which results in lower leptin transport across the BBB . Although leptin is secreted principally by adipocytes, Wiesner et al have identified the brain as a producer of leptin by measuring of transcerebral leptin flux.…”

Section: Introductionmentioning

confidence: 99%

Differential physiological responses to central leptin overexpression in male and female rats

Côté

Green

Toklu

et al. 2017

J Neuroendocrinology

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Brains of females are more sensitive to the acute catabolic actions of leptin. However, sex differences in the long-term physiological responses to central leptin receptor modulation are unknown. To this end, we centrally delivered a viral vector to overexpress leptin (Leptin), a neutral leptin receptor antagonist (Leptin-Antagonist), or a green fluorescence protein (Control). We examined chronic changes in body weight and composition in male and female rats. Females displayed greater and sustained responses to Leptin whereas males rapidly lost physiological effects and developed leptin resistance confirmed by lower acute leptin-mediated phosphorylation of STAT3 (P-STAT3). Surprisingly, despite persistent physiological responses, Leptin-females also exhibited reduced acute leptin-mediated P-STAT3, suggesting an onset of leptin resistance near time of death. In line with this interpretation, Leptin-females and Control-females consumed the same amount of food on the last day of the experiment. Both Leptin-Antagonist groups gained similar percentages of their initial body weight and fat mass, whereas only Leptin-Antagonist-females gained lean body mass. Consequently, lean/fat mass ratio with Leptin-Antagonist was preserved in females and decreased in males, suggesting a deterioration of body composition in males. In summary, this study establishes that females are more responsive to long-term central leptin overexpression than males and that leptin antagonism has a greater physiological impact in males. The hormone environment may have played a role in these processes; however, future studies are needed to establish whether physiological responses are mediated by female or male sex hormones.

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“…Although there are at least six alternatively spliced isoforms of the leptin receptor (Lep-Ra, Rb, Rc, Rd, Re and Rf) in mice [7] , it is activation of Lep-Rb that is reported to be most involved in metabolic control. The shorter isoforms are thought to act as leptin transporters at different sites, including plasma and the blood-brain barrier [8,9] .…”

Section: Introductionmentioning

confidence: 99%

Leptin in Early Life: A Key Factor for the Development of the Adult Metabolic Profile

Granado¹,

Fuente-Martín²,

García‐Cáceres³

et al. 2012

Obes Facts

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Leptin levels during the perinatal period are important for the development of metabolic systems involved in energy homeostasis. In rodents, there is a postnatal leptin surge, with circulating leptin levels increasing around postnatal day (PND) 5 and peaking between PND 9 and PND 10. At this time circulating leptin acts as an important trophic factor for the development of hypothalamic circuits that control energy homeostasis and food seeking and reward behaviors. Blunting the postnatal leptin surge results in long-term leptin insensitivity and increased susceptibility to diet-induced obesity during adulthood. Pharmacologically increased leptin levels in the postnatal period also have long-term effects on metabolism. Nevertheless, this effect is controversial as postnatal hyperleptinemia is reported to both increase and decrease the predisposition to obesity in adulthood. The different effects reported in the literature could be explained by the different moments at which this hormone was administered, suggesting that modifications of the neonatal leptin surge at specific time points could selectively affect the development of central and peripheral systems that are undergoing modifications at this moment resulting in different metabolic and behavioral outcomes. In addition, maternal nutrition and the hormonal environment during pregnancy and lactation may also modulate the offspring's response to postnatal modifications in leptin levels. This review highlights the importance of leptin levels during the perinatal period in the development of metabolic systems that control energy homeostasis and how modifications of these levels may induce long-lasting and potentially irreversible effects on metabolism.

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Developmental increases in plasma leptin binding activity and tissue Ob-Re mRNA expression in the rat

Cited by 14 publications

References 47 publications

Sex differences in the physiology of eating

Sex differences in the physiology of eating

Differential physiological responses to central leptin overexpression in male and female rats

Leptin in Early Life: A Key Factor for the Development of the Adult Metabolic Profile

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