AREGU August 46/2
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چکیده
Mantha, Line, Elena Palacios, and Yves Deshaies. Modulation of triglyceride metabolism by glucocorticoids in diet-induced obesity. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R455–R464, 1999.—The involvement of glucocorticoids (GC) in the development of diet-induced obesity and in the concomitant adaptations of triglyceride (TG)-rich lipoprotein metabolism were examined. Rats were fed either rodent chow, which maintains a low lipid flux, or a diet high in sucrose and fat (HSF) that increases lipid flux, leading to metabolic perturbations similar to those that define the plurimetabolic syndrome in humans. The GC status was manipulated through adrenalectomy (ADX) and corticosterone (Cort) replacement. Compared with chow, the HSF diet increased energy intake (17%) and whole body (8%) and adipose tissue (80%) weights. The HSF diet also increased the acute postprandial rise in plasma insulin (4-fold) and TG (3-fold), fasting liver TG content (3-fold), triglyceridemia (54%), and adipose tissue lipoprotein lipase (LPL) activity (2-fold). ADX decreased energy intake and whole body and adipose tissue weights in both dietary cohorts, but more so in HSF-fed than in chow-fed animals. These ADX-induced effects were totally prevented by Cort replacement in rats fed chow, but only partially so in those fed the HSF diet in proportion to the degree of restoration of energy intake. In the chow-fed cohort, the above indexes of TG metabolism remained unaffected by the Cort status, whereas in the HSF-fed cohort, these variables were decreased by ADX to levels of chow-fed animals. Cort replacement in the HSF-fed animals restored indexes of TG metabolism to intact levels and reestablished the diet-related differences observed in intact animals. These findings indicate that GC modulate fasting TG metabolism only minimally when a diet that maintains a low lipid flux is fed. In contrast, their presence is a necessary condition for the development of diet-induced obesity and the concomitant alterations in insulin sensitivity and TG-rich lipoprotein metabolism.
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AREGU August 46/2
Duan, Yu-Fei, Irwin J. Kopin, and David S. Goldstein. Stimulation of the paraventricular nucleus modulates firing of neurons in the nucleus of the solitary tract. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R403–R411, 1999.—The present study assessed whether the baroreflex inhibition elicited by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) involve...
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Saito, Takako, San-e Ishikawa, Sei Sasaki, Minori Higashiyama, Shoichiro Nagasaka, Nobuya Fujita, Kiyohide Fushimi, Fumiaki Marumo, and Toshikazu Saito. Lack of vasopressin-independent upregulation ofAQP-2 gene expression in homozygous Brattleboro rats. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R427–R433, 1999.—Arginine vasopressin (AVP) plays an important role in the expr...
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Moran, Daniel S., John W. Castellani, Catherine O’Brien,Andrew J. Young, and Kent B. Pandolf. Evaluating physiological strain during cold exposure using a new cold strain index. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R556–R564, 1999.—A cold strain index (CSI) based on core (Tcore) and mean skin temperatures (Tsk) and capable of indicating cold strain in real time and an...
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