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Preabsorptive and postabsorptive signals from the gastrointestinal tract and changes in plasma nutrient levels provide short- and long-term feedback to regulate food intake:

• Gastrointestinal hormones (eg, glucagon-like peptide 1 [GLP-1], cholecystokinin [CCK], peptide YY [PYY]) reduce food intake.

• Ghrelin, secreted primarily by the stomach, increases food intake.

• Leptin, secreted from adipose tissue, informs the brain how much fat is stored. Leptin suppresses appetite in normal-weight people, but high leptin levels correlate with increased body fat. Leptin levels can decrease when weight is lost and then send a hunger signal to the brain.

The hypothalamus integrates various signals involved in the regulation of energy balance and then activates pathways that increase or decrease food intake:

• Neuropeptide Y (NPY), agouti-related peptide (ARP), alpha-melanocyte–stimulating hormone (alpha-MSH), cocaine- and amphetamine-related transcript (CART), orexin, and melanin-concentrating hormone (MCH) increase food intake.

• Corticotropic hormone (CRH) and urocortin decrease it.

The limbic system (amygdala, hippocampus, and prefrontal cortex) mediates the hedonistic pathway for food intake, including cravings, habit, and reward. The desire to eat can override homeostatic pathways because emotion and stress have been shown to affect regulatory peptides such as ghrelin. These effects are mediated by dopamine.