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Central nervous system control of food intake
TLDR
A model is described that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
Hypothalamic mTOR Signaling Regulates Food Intake
TLDR
It is demonstrated that mTOR signaling plays a role in the brain mechanisms that respond to nutrient availability, regulating energy balance, and that hypothalamic activity is directly tied to the regulation of energy intake.
Identification of targets of leptin action in rat hypothalamus.
TLDR
The findings suggest that leptin action in rat hypothalamus involves altered expression of key neuropeptide genes, and implicate leptin in the hypothalamic response to fasting.
Signals that regulate food intake and energy homeostasis.
TLDR
This review focuses on the molecular signals that modulate food intake while integrating the body's immediate and long-term energy needs.
A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women.
TLDR
A very low carbohydrate diet is more effective than a low fat diet for short-term weight loss and, over 6 months, is not associated with deleterious effects on important cardiovascular risk factors in healthy women.
The Hunger Games
TLDR
Direct imaging in vivo of AgRP and POMC neurons in the hypothalamus is used to demonstrate rapid changes in their activity upon food presentation, which challenges classic notions of their functions and raises new hypotheses.
Leptin Increases Hypothalamic Pro-opiomelanocortin mRNA Expression in the Rostral Arcuate Nucleus
TLDR
The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors, and supports the hypothesis that leptin signaling in the brain involves activation of the hypothalamic melanocortin system.
Mice lacking ghrelin receptors resist the development of diet-induced obesity.
TLDR
It is shown that when fed a high-fat diet, both female and male GHSR-null mice eat less food, store less of their consumed calories, preferentially utilize fat as an energy substrate, and accumulate less body weight and adiposity than control mice, which supports the hypothesis that ghrelin-responsive pathways are an important component of coordinated body weight control.
Insulin activation of phosphatidylinositol 3-kinase in the hypothalamic arcuate nucleus: a key mediator of insulin-induced anorexia.
TLDR
The hypothesis that the IRS-PI3K pathway is a mediator of insulin action in the arcuate nucleus is supported and, combined with recent evidence that leptin activates PI3K signaling in the hypothalamus, provide a plausible mechanism for neuronal cross-talk between insulin and leptin signaling.
Specificity of Leptin Action on Elevated Blood Glucose Levels and Hypothalamic Neuropeptide Y Gene Expression in ob/ob Mice
TLDR
In ob/ob mice, systemic administration of leptin inhibits NPY gene overexpression through a specific action in the arcuate nucleus and exerts a hypoglycemic action that is partly independent of its weight-reducing effects.
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