Leptin is an adipocyte-derived blood-borne satiety factor that acts directly on the hypothalamus, thereby regulating food intake and energy expenditure. We have demonstrated that the hypothalamic arcuate nucleus (Arc) is a primary site of the satiety effect of leptin (Neurosci Lett 224:149-152, 1997). To explore the hypothalamic pathway of sympathetic activation of leptin, we examined the effects of a single intravenous or intracerebroventricular injection of recombinant human leptin on catecholamine secretion in rats. We also examined the effects of direct microinjection of leptin into the ventromedial hypothalamus (VMH), Arc, paraventricular nucleus (PVN), and dorsomedial hypothalamus (DMH) in rats. To further assess whether sympathetic activation of leptin is mediated via the VMH, we also examined the effects of a single intravenous injection of leptin in VMH-lesioned rats. A single injection of leptin (0.25-1.0 mg i.v./rat or 0.5-2.0 pg i.c.v./rat) increased plasma norepinephrine (NE) and epinephrine (EPI) concentrations in a dose-dependent manner. Plasma NE and EPI concentrations were increased significantly when leptin was injected directly into the VMH but were unchanged when injected into the Arc, PVN, and DMH. Plasma NE and EPI concentrations were unchanged in VMH-lesioned rats that received a single intravenous injection of leptin. The present study provides evidence that a leptin-induced increase in catecholamine secretion is mediated primarily via the VMH and suggests the presence of distinct hypothalamic pathways mediating the satiety effect and sympathetic activation of leptin.

Abstract-Adrenomedulhn(AM), a potent vasodllator peptlde, exists m the cardiac ventricle, however, the role of AM m the ventricular tissue remams unknownIn the present study, we mvestlgated the production and secretlon of AM m cultured neonatal rat cardlomyocytes, and we exammed the effect of AM on de novo protein synthesis m these cells by measurmg ['4C] any efforts have been made to clarify the mechanisms of growth regulation of the cardiac myocardmm because of comphcatlons of the heart caused by cardiac hypertrophy At the cellular level, cardiac myocytes are known to compensate for increased workload by an Increase m their size but not m their number because these cell? are unable to dlvlde later m life ' Multiple factors such as hemodynamlc overload and humoral factors were shown to be mvolved m the process of the cardiac hypertrophy,2-4 but the detailed mechanism remams to be elucidated AM, a potent vasodllator peptlde first detected m human pheochromocytoma, has slight homology with CGRP' In addltlon to the direct vasodllator actlvlty, AM has been shown to possess a broad spectrum of blologlcal actions such as dluresls, mhlbltlon of aldosterone secretion, and mhlbltlon of prohferatlon of vascular smooth muscle cells '-* A specific RIA revealed that AM circulates m the blood and 1s present m the adrenal medulla, kidney, lung and cardiac ventricle of humans and rats ')I" The plasma AM concentration m patients with essential hypertension or primary aldosteromsm was reported to be higher than that m normotenslve control subjects, suggesting a possible role of AM m acting against further elevation of blood pressure "J' In the cardiac ventricle, AM mRNA 1s expressed at a level comparable to that of the adrenal medulla,'3b'4 and both the AM content and mRNA expression are increased m Dahl salt-sensmve and renovascular hypertensive rats compared to respective controls I516 However, at present, It remains unknown whether the cardiac myocytes secrete AM, and what the role of AM 1s m the cardiac tissueIn the first part of this study, we exammed the production and secretion of AM from cultured neonatal cardiac myocytes In the second, we investigated the effect ofAM on the de novo protein synthesis m these cells by measurmg ['4C]phenylalanme mcorporatlon, and we evaluated the action of endogenous AM by using a peptlde analogue of CGRP and anti-AM monoclonai antibody Chemicals Methods Ang II, rat AM, human

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The "Yubi-wakka" test is an extremely practical method to identify older adults at risk of sarcopenia, disability and mortality. This test might contribute to increased primary prevention for sarcopenia by serving as an early wake-up call for older adults against becoming sarcopenic. Geriatr Gerontol Int 2018; 18: 224-232.