Research
Hormonal
Short-term food intake regulation is driven by a 'glucostatic' mechanism where glucose utilization in the ventromedial hypothalamus triggers satiety, rather than blood glucose concentration alone.
Focus on how your body uses carbohydrates (glucose utilization) rather than just avoiding them. The brain's ability to process glucose signals satiety.
GoodSupportsHIGH confidence
The 'glucostatic' hypothesis was based in part on the observation that carbohydrate reserves are proportionately much more depleted between meals than are reserves of protein or fat.
Why this rating
Supported by correlation studies, glucagon administration, and lesion studies.
Source
Regulation of Food Intake and Obesity
Jean Mayer et al. · Science · 1967
DOI 10.1126/science.156.3773.328
narrative_reviewCited 313×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Obesity results from a failure of the central hypothalamic satiety mechanism (specifically the ventromedial nucleus) to inhibit the lateral feeding center, leading to hyperphagia, rather than from a simple failure of peripheral stomach sensations.Good
- The ventromedial nucleus of the hypothalamus acts as a 'satiety center' that inhibits the lateral 'feeding center'; destruction of this area causes hyperphagia and obesity due to a failure to terminate feeding, not an increase in the motivation to start eating.Good
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