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Brain Res Bull. 1986 Oct;17(4):563-9.

Hyperprolactinemia stimulates food intake in the female rat.


Lactation in the rat is marked by extreme hyperphagia. The present study examined the possibility that elevated prolactin levels contribute to this increase. It also evaluated the effects of hyperprolactinemia on brown adipose tissue and carcass composition. Virgin Osborne-Mendel rats were made hyperprolactinemic via ectopic pituitary transplants (PIT, n = 9) or were sham-operated (SHAM, n = 8). Eight lactating rats (LACT) served as additional controls. Food intake, body weight and rectal temperature were recorded daily. Eleven days postsurgery (or 11-12 days postpartum), the rats were sacrificed, and brown fat (scapular, axillary, cervical and thoracic) was excised, weighed, and assayed for GDP binding, one indicator of thermogenic capacity. Carcasses were subjected to body composition analysis. Although prior to surgery, PIT and SHAM rats weighed the same, PIT rats gained significantly more weight during the experiment than did SHAMs. Percent body fat and food intake (both total intake and intake relative to metabolic body size) were significantly elevated in the PIT rats. GDP binding in both PIT and LACT rats was significantly less than in SHAMs. This was true whether GDP binding was expressed per mg mitochondrial protein or per total amount of mitochondrial protein recovered. These data confirm that brown fat thermogenic capacity is suppressed during lactation. They also demonstrate that elevations of serum prolactin, to levels that are well within physiological limits, are capable of stimulating food intake and white fat deposition in the female rat. It is presently unclear whether these results are a direct or an indirect effect of hyperprolactinemia.

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