Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increases in serum estrogen inhibit food intake. Conversely, progesterone stimulates food intake, probably via its antiestrogenic action. We have reported that elevated serum prolactin also stimulates food intake in female rats. It is unclear whether this effect is mediated through elevated levels of progesterone. The present study investigated the effects of prolactin on food intake and brown fat activity in the absence of progesterone. Female Osborne-Mendel rats were assigned to one of six groups: sham operated (Sham, n = 10), ovariectomized (OVX, n = 10), OVX + low estrogen (EL, n = 11), OVX + EL + prolactin (PIT, n = 9), OVX + high estrogen (EH, n = 10), and OVX + EH + PIT (n = 8). Estrogen levels were elevated by Silastic implants. Prolactin levels were elevated through pituitary transplants placed under the kidney capsule. Nine days postsurgery, food intake was significantly higher in OVX vs. Sham rats. Estrogen-treated rats (OVX + EL and OVX + EH) had significantly suppressed food intake values compared with both Sham and OVX animals. Finally, hyperprolactinemic rats (OVX + EL + PIT and OVX + EH + PIT) ate significantly more food than did estrogen-treated rats without pituitary explants. Despite the hyperphagia, no significant differences in brown fat GDP binding were observed. These data indicate that prolactin stimulates food intake in the absence of ovarian progesterone.
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PMID:Prolactin stimulates food intake in the absence of ovarian progesterone. 292 59

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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PMID:Hyperprolactinemia stimulates food intake in the female rat. 377 56

Continually rising global obesity rates present a major challenge to human health. The contribution of Pavlovian motivational processes to overeating and obesity has become increasingly apparent. In humans, brain and behavioral reactivity to food-related stimuli positively correlates with subsequent weight gain. In concordance with this, selectively bred obesity-prone rats show stronger single-outcome Pavlovian-to-instrumental transfer (SO PIT) than obesity-resistant rats, providing support for the hypothesis that enhanced Pavlovian motivation is a pre-existing phenotype of obesity-susceptibility. However, whether obesity-susceptibility in outbred rats is associated with similar enhancements in PIT was unknown. Moreover, given that SO PIT does not distinguish between sensory specific and general affective motivational processes, it was unclear which of these was linked to obesity-susceptibility. Thus, here we determined whether obesity-susceptibility is associated with enhanced Sensory Specific (SS) PIT versus General PIT using both outbred and selectively bred populations. Rats were trained with two action-outcome and three stimulus-outcome associations; two of the Pavlovian and instrumental associations shared a common outcome. During PIT testing, the influence of the Pavlovian stimuli on the two instrumental responses were measured simultaneously. In outbred rats, expression of General PIT was positively correlated with subsequently determined obesity-susceptibility. In selectively bred rats, General PIT was stronger in obesity-prone versus obesity-resistant rats. Jointly, these data show that enhanced affective Pavlovian motivation is tightly linked to obesity vulnerability, supporting a role for phenotypic differences in incentive motivation in vulnerability to obesity. This has important implications for obesity prevention and for the specific neurocircuitry underlying enhanced food-seeking in vulnerable populations.
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PMID:Affective Pavlovian motivation is enhanced in obesity susceptible populations: Implications for incentive motivation in obesity. 3176 Jan 53