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      Effect of Naltrexone on Feeding, Neuropeptide Y and Uncoupling Protein Gene Expression during Lactation

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          Neuropeptide Y increases feeding and decreases measures of brown adipose tissue thermogenesis. In lactating rats, increased feeding, increased hypothalamic neuropeptide Y neuroactivity and decreased thermogenesis occur. Naltrexone is an opioid receptor antagonist which decreases neuropeptide Y-induced feeding and reverses neuropeptide Y-induced decreases in brown adipose tissue thermogenesis. We hypothesized that opioid receptors are involved in neuropeptide Y neuroactivity during lactation. To see if naltrexone would alter feeding, neuropeptide Y gene expression in the arcuate nucleus, neuropeptide Y levels in the paraventricular nucleus, and uncoupling protein gene expression in brown adipose tissue of lactating rats, osmotic minipumps pre-filled with either 0.9% saline or naltrexone (70 µg/h) were implanted subcutaneously in 47 female Sprague-Dawley rats weighing 309 ± 5 g. Half these rats were studied on days 10–16 of lactation, and the other half were studied 7 days after lactation. After 48 h, neuropeptide Y mRNA levels and uncoupling protein mRNA levels were determined using specific cDNA probes. Neuropeptide Y peptide levels in the paraventricular nucleus were measured by radioimmunoassay. Naltrexone decreased food intake by 26% in the post-lactating rats, but had no effect on feeding in the lactating animals. Lactation resulted in significantly increased arcuate neuropeptide Y mRNA, decreased neuropeptide Y levels in the paraventricular nucleus and decreased brown adipose tissue uncoupling protein mRNA levels. Naltrexone did not influence any of these parameters. Thus, the alterations in neuropeptide Y neuroactivity and brown fat thermogenesis which occur in lactation is not altered by generalized opioid receptor blockade.

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          Author and article information

          S. Karger AG
          09 April 2008
          : 65
          : 4
          : 259-264
          Departments of Food Science and Nutrition, Psychiatry and Medicine, University of Minnesota, Saint Paul, Minn, and Veterans Affairs Medical Center, Minneapolis, Minn., USA
          127183 Neuroendocrinology 1997;65:259–264
          © 1997 S. Karger AG, Basel

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          Page count
          Pages: 6
          Physiology of Hypothalamic Neurons


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