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Response of plasma leptin concentration to jugular infusion of glucose or lipid is dependent on the stage of lactation of Holstein cows.

作者信息

Chelikani Prasanth K, Keisler Duane H, Kennelly John J

机构信息

Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5.

出版信息

J Nutr. 2003 Dec;133(12):4163-71. doi: 10.1093/jn/133.12.4163.

Abstract

In this study we investigated the hormonal and metabolite responses to isoenergetic jugular infusions of glucose or lipid in early- and late-lactation Holstein cows. Six Holstein cows were used in a replicated Latin square design with jugular infusions of either 1) control (CON; saline), 2) glucose (GLU; 50% dextrose) or 3) lipid (LIP; 20% Intralipid). Treatments did not affect dry matter intake, with the exception of a hypophagic effect of LIP in late lactation. The GLU-induced hyperglycemia and hyperinsulinemia were greater in late-lactation than in early-lactation cows. The GLU treatment did not affect plasma leptin and insulin-like growth factor-1 (IGF-1) concentrations in early-lactation cows, but it increased them in late-lactation cows. The LIP treatment did not affect plasma leptin, insulin and IGF-1 concentrations in early-lactation cows, despite a marked LIP-induced increase in plasma nonesterified fatty acid and beta-hydroxybutyrate concentrations and a reduction in growth hormone (GH) concentration. Compared with the delayed leptin response to GLU, the stimulatory effect of LIP on leptin secretion in late-lactation cows was relatively rapid and occurred in the absence of any significant changes in plasma insulin, IGF-1 or GH. We propose that insulin-mediated glucose metabolism may be involved in the stimulatory effects of glucose on leptin secretion in late-lactation animals but that the stimulatory effects of lipid are independent of insulin or IGF-1. In early-lactation animals a strong inhibitory effect of GH on leptin expression and release, in addition to low adipose reserves and/or energy balance, might override any short-term stimulatory effect of glucose or lipid on leptin secretion.

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