Article

Insulin, leptin, and food reward: Update 2008

Metabolism/Endocrinology (151) VA Puget Sound Health Care System, 1660 So. Columbian Way, Seattle, WA 98108, USA.
AJP Regulatory Integrative and Comparative Physiology (Impact Factor: 3.11). 11/2008; 296(1):R9-R19. DOI: 10.1152/ajpregu.90725.2008
Source: PubMed

ABSTRACT

The hormones insulin and leptin have been demonstrated to act in the central nervous system (CNS) as regulators of energy homeostasis at medial hypothalamic sites. In a previous review, we described new research demonstrating that, in addition to these direct homeostatic actions at the hypothalamus, CNS circuitry that subserves reward and motivation is also a direct and an indirect target for insulin and leptin action. Specifically, insulin and leptin can decrease food reward behaviors and modulate the function of neurotransmitter systems and neural circuitry that mediate food reward, i.e., midbrain dopamine and opioidergic pathways. Here we summarize new behavioral, systems, and cellular evidence in support of this hypothesis and in the context of research into the homeostatic roles of both hormones in the CNS. We discuss some current issues in the field that should provide additional insight into this hypothetical model. The understanding of neuroendocrine modulation of food reward, as well as food reward modulation by diet and obesity, may point to new directions for therapeutic approaches to overeating or eating disorders.

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    • "This endocrine signal reflecting the metabolic need then affects the interaction between orexigenic and anorexigenic hypothalamic and hindbrain circuits [31] [42]. The withdrawal of leptin inhibition over the ventral pallidal hunger circuit when its reduced basal concentration reflects declines in body fat mass was shown to contribute to increased desirability or incentive salience of food [3] [15] [20] [36]. The hormonal mediation of hunger is further supported by the temporal concordance between increases in hunger and concentrations of the gastric hormone ghrelin during the interval preceding spontaneous meals and decreases in both variables upon food ingestion [10] and by suppression of hunger after intravenous infusion of supra-physiological concentrations of the hormone [44]. "

    Full-text · Dataset · Sep 2014
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    • "This endocrine signal reflecting the metabolic need then affects the interaction between orexigenic and anorexigenic hypothalamic and hindbrain circuits [31] [42]. The withdrawal of leptin inhibition over the ventral pallidal hunger circuit when its reduced basal concentration reflects declines in body fat mass was shown to contribute to increased desirability or incentive salience of food [3] [15] [20] [36]. The hormonal mediation of hunger is further supported by the temporal concordance between increases in hunger and concentrations of the gastric hormone ghrelin during the interval preceding spontaneous meals and decreases in both variables upon food ingestion [10] and by suppression of hunger after intravenous infusion of supra-physiological concentrations of the hormone [44]. "

    Full-text · Dataset · Sep 2014
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    • "Leptin decreases responses related to food reward through actions mediated by the midbrain dopamine and opioidergic pathways, effects that may result in alterations in food preference [36,37]. Two months following discontinuation of the leptin infusion, a diet preference test showed no differences between LEP and PBS mice when offered both 10% and 30% fat diets ad-libitum (Figure 5). "
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    ABSTRACT: Circulating leptin concentrations correlate with fat mass and signal the status of somatic energy stores to the brain. Previous studies suggest that diet-induced elevations of body weight increase body weight “set-point”. To assess whether chronic hyperleptinemia is responsible for this shift in defended body weight, we elevated circulating leptin concentrations in lean mice to those comparable to diet-induced obese mice for eighteen weeks. We hypothesized that following cessation of leptin infusion, a higher body weight would be defended. Compared to saline-infused controls, leptin-infused mice had elevated circulating leptin concentrations, gained less weight, yet had similar metabolic rates. Following cessation of leptin administration, leptin-infused mice gained some weight yet plateaued at 5-10% below controls. These results suggest that, unlike mice rendered hyperleptinemic by diet-induced weight gain, leptin-infused mice do not subsequently “defend” a higher body weight, suggesting that hyperleptinemia per se does not mimic the CNS consequences of chronic weight gain.
    Full-text · Article · Jul 2014 · Molecular Metabolism
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