Hormonal
Administration of the fatty acid synthase inhibitor C75 reduces food intake and body weight in mice by inhibiting hypothalamic AMP-activated protein kinase (AMPK) activity, thereby decreasing neuropeptide Y (NPY) expression.
This research identifies a specific brain pathway where inhibiting fatty acid synthesis reduces hunger. While C75 itself is a research chemical and not a consumer supplement, the findings suggest that strategies which influence hypothalamic energy sensing (like AMPK activity) could be key to managing appetite. Current practical advice remains focused on sustainable dietary habits, but this highlights the biological complexity of hunger regulation.
C75, a fatty acid synthase (FAS) inhibitor, causes weight loss and anorexia... C75 rapidly reduced the level of the phosphorylated AMPK beta subunit (pAMPKbeta) in the hypothalamus... C75 reduced the levels of pAMPKbeta and phosphorylated cAMP response element-binding protein (pCREB) in the arcuate nucleus neurons of the hypothalamus, suggesting a mechanism for the reduction in NPY expression seen with C75 treatment.
Why this rating
The study is a rigorous mechanistic investigation in mice (in vivo) with clear dose-response and reversal experiments, but it lacks human clinical data.
Source
C75, a Fatty Acid Synthase Inhibitor, Reduces Food Intake via Hypothalamic AMP-activated Protein Kinase
Eun Kyoung Kim et al. · Journal of Biological Chemistry · 2004
DOI 10.1074/jbc.m402165200
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