The arcuate nucleus as a primary site of satiety effect of leptin in rats

Satoh, Noriko; Ogawa, Yoshihiro; Katsuura, Goro; Hayase, Minoru; Tsuji, Tetsuo; Imagawa, Keiichi; Yoshimasa, Yasunao; Nishi, Shogo; Hosoda, Kiminori; Nakao, Kazuwa

doi:10.1016/s0304-3940(97)00163-8

Cited by 191 publications

(102 citation statements)

References 24 publications

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“…The hypothalamus is known to be the center for hunger and satiety [36] . In particular, the arcuate nucleus of the hypothalamus is activated by ghrelin administration and this region is known to have important role in controlling food intake relating to the action of leptin [37] . Date et al [12] indicated that Ⅳ injection of ghrelin induces Fos expression in neuropeptide Y (NPY)-producing and growth hormone-releasing hormone (GHRH)-producing neurons in the arcuate neucleus.…”

Section: Central Regulation Of Gastric Acid Secretion By Ghrelinmentioning

confidence: 99%

Ghrelin and gastric acid secretion

Yakabi¹,

Kawashima²,

Kato³

2008

WJG

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Section: Central Regulation Of Gastric Acid Secretion By Ghrelinmentioning

confidence: 99%

Ghrelin and gastric acid secretion

Yakabi¹,

Kawashima²,

Kato³

2008

WJG

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“…There is increasing evidence that the hypothalamus is one of the targets for leptin. 9,10 Besides leptin, proopiomelanocortin signaling in the hypothalamus has been implicated in energy balance. [11][12][13] It has also been shown that tar- geted mutation of melanocortin-4 receptor caused obesity in mice.…”

Section: Brs-3 Deficient Micementioning

confidence: 99%

Bombesin, obesity, and social behavior

Wada

Watase

et al. 1998

Mol Psychiatry

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The bombesin system has not been very well characterized in the brain. This may be due to a lack of specific antagonists or agonists or to the diversity of physiological effects of bombesin. Bombesin receptors are phylogenetically most related to endothelin receptors whose importance is well-known. Our studies on bombesin receptor knock-out mice indicate the necessity and potential fruitfulness of further efforts to examine in detail the role of bombesin in brain function.

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Section: Introductionmentioning

confidence: 96%

“…The biologic actions of leptin are thought to be mediated through the activation of leptin receptor that is expressed in the hypothalamus (16)(17)(18)(19). We and others demonstrated that the hypothalamic arcuate nucleus is a primary site of the satiety effect of leptin (20,21) and that its satiety effect is mediated at least partly by hypothalamic melanocortin system (22,23).Numerous studies have demonstrated that plasma leptin concentrations are elevated significantly in several models of rodent obesity and in human obesity in proportion to the degree of adiposity (24-26), suggesting the state of "leptin resistance" in obesity. Nevertheless, because of the potent pleiotropic actions of leptin, it is conceivable, though paradoxically, that hyperleptinemia may be involved in the pathogenesis of obesity and its related disorders.…”

mentioning

confidence: 95%

Pathophysiological role of leptin in obesity-related hypertension

Aizawa-Abe¹,

Ogawa²,

Masuzaki³

et al. 2000

J. Clin. Invest.

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437

312

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IntroductionObesity is defined as increased mass of adipose tissue and confers a higher risk of arterial blood pressure (BP) elevation or hypertension (1-4). On the other hand, weight reduction lowers BP in obese hypertensive subjects (5-8), suggesting an important association between energy homeostasis and BP. However, the mechanism for that association is poorly understood. Obesity-related hypertension may be secondary to insulin resistance and/or hyperinsulinemia (2,3,8). Several lines of evidence have also suggested that increased sympathetic nerve activity may contribute to the development of obesity-related hypertension (2, 6, 7).The adipose tissue participates in the regulation of a variety of homeostatic processes as an endocrine organ that secretes many biologically active molecules such as FFA, adipsin, angiotensinogen,. Leptin is such an adipocyte-derived hormone that is involved in the regulation of food intake and body weight (10). It also increases the overall sympathetic nerve activity, which leads to a significant increase in energy expenditure (11-15). The biologic actions of leptin are thought to be mediated through the activation of leptin receptor that is expressed in the hypothalamus (16)(17)(18)(19). We and others demonstrated that the hypothalamic arcuate nucleus is a primary site of the satiety effect of leptin (20,21) and that its satiety effect is mediated at least partly by hypothalamic melanocortin system (22,23).Numerous studies have demonstrated that plasma leptin concentrations are elevated significantly in several models of rodent obesity and in human obesity in proportion to the degree of adiposity (24-26), suggesting the state of "leptin resistance" in obesity. Nevertheless, because of the potent pleiotropic actions of leptin, it is conceivable, though paradoxically, that hyperleptinemia may be involved in the pathogenesis of obesity and its related disorders. In this regard, a recent study reported a significant correlation between BP and plasma leptin concentrations in patients with essential hypertension (27), suggesting that leptin may play roles in the pathogenesis of obesity-related hypertension.We have recently produced transgenic skinny mice overexpressing leptin under the control of the liver-specific promoter and demonstrated that chronic hyperleptinemia results in complete disappearance of adipose tissue for a long period (28). These mice also exhibit increased glucose metabolism and insulin sensitivity, accompanied by an activation of insulin signaling in the skeletal muscle and liver (28,29). Accordingly, transgenic skinny mice will serve as the unique experimental model system with which to assess the long-term effects of leptin in vivo. To explore the pathophysiological role of leptin in obesity-related hypertension, we examined cardiovascular phenotypes of transgenic skinny mice whose elevated plasma leptin concentrations are comparable to those seen in obese subjects. We also studied genetically obese KKA y mice with hyperleptinemia, in which hypothalamic melano...

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The arcuate nucleus as a primary site of satiety effect of leptin in rats

Cited by 191 publications

References 24 publications

Ghrelin and gastric acid secretion

Ghrelin and gastric acid secretion

Bombesin, obesity, and social behavior

Pathophysiological role of leptin in obesity-related hypertension

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