Weight Loss

The cell's master energy sensor — when fuel runs low it ignites fat-burning, glucose uptake and mitochondrial renewal while standing down growth. Evidence A — Human trial evidence.

How much body fat you carry, shown by body weight, BMI and waist size. Higher means more fat. Where fat sits matters too: fat around the belly and organs (visceral fat) carries more health risk than fat under the skin, and muscle is tracked separately. Evidence A — Human trial evidence.

Fatty-acid synthesis — the de-novo line that converts surplus carbohydrate into stored fat and liver triglyceride. Evidence A — Human trial evidence.

A protein called UCP1 lets a fat cell release energy as heat rather than bank it — real, measurable, and smaller than the internet believes. Evidence B — Preclinical.

The mitochondrial pathway that dismantles fatty acids into cellular energy — the engine that empties stored and circulating fat. Evidence A — Human trial evidence.

Adipogenesis — the process by which a precursor cell commits to becoming a new fat cell. Evidence A — Human trial evidence.

Gut hormone for appetite control and steady blood sugar. Evidence A — Human trial evidence.

GLP-1 — the incretin hormone that sharpens glucose-dependent insulin release and signals satiety.

Cell turnover — the orderly self-removal that clears damaged and worn-out cells so the tissue renews instead of accumulating them. Evidence A — Human trial evidence.

The signal that a meal is enough. Most published studies measure hunger and AgRP drive — satiety's absence — so their direction is read inverted here, and that is said openly. Evidence A — Human trial evidence.

Insulin sensitivity — how readily cells respond to insulin, the linchpin of metabolic health. Evidence B — Preclinical.

Fasting insulin — a sensitive marker of insulin resistance; chronically high levels signal metabolic strain. Evidence A — Human trial evidence.

An adipose-derived hormone that sharpens insulin sensitivity and steers fat toward burning rather than storage. Evidence A — Human trial evidence.

Makes the first cut into stored fat, the step that sets the pace. Evidence B — Preclinical.

The ketone body the liver makes when glucose runs low — an alternative fuel that doubles as an anti-inflammatory signaling molecule. Evidence B — Preclinical.

Cholecystokinin — released by the upper small intestine when fat and protein arrive, it slows the stomach and tells the brain the meal is done. Evidence A — Human trial evidence.

C/EBP-alpha — the transcription factor that works with PPAR-gamma to commit a precursor cell to becoming a fat cell.

The mitochondrial pathway that dismantles fatty acids into cellular energy.

Gastric emptying — the rate at which a meal leaves the stomach. Slower emptying means fullness lasts longer and glucose arrives more gently. Evidence B — Preclinical.

The lipase the adrenaline signal actually phosphorylates. It takes the second bond ten times better than the first — and it also manufactures the signal that keeps fat cells healthy. Evidence B — Preclinical.

The step where stored fat actually leaves the fat cell — triglyceride split into fatty acids and glycerol, and let out into the blood. Evidence B — Preclinical.

The metabolic intermediate that signals fuel abundance by clamping the mitochondrial fat-import gate shut. Evidence B — Preclinical.

The coat protein over stored fat that holds the fat-releasing machinery back until it is told to let go. Evidence B — Preclinical.

The kinase that actually opens the fat droplet — it phosphorylates the coat protein guarding the fat and the lipase that cuts it. Evidence B — Preclinical.

The satiety hormone from fat tissue. The decisive fact: in common obesity leptin is high, not low — the problem is resistance to the signal, so replacement logic fails. The evidence shows the case where it worked and the disqualifier beside it. Evidence B — Preclinical.

Visceral adipose tissue — the fat packed around the abdominal organs, the metabolically active depot that drives insulin resistance and inflammation.

Acts on 10 of these pathways: Weight & Body Fat, Mitochondrial Uncoupling, Incretin, Satiety, Insulin Sensitivity, Fasting Insulin, Adiponectin, Cholecystokinin, Gastric Emptying, Leptin Signaling.

Acts on 9 of these pathways: AMPK, Weight & Body Fat, Fatty-Acid Synthesis, Mitochondrial Uncoupling, Fatty-Acid β-Oxidation, Insulin Sensitivity, Fasting Insulin, β-Hydroxybutyrate, Malonyl-CoA.

Acts on 8 of these pathways: AMPK, Weight & Body Fat, Mitochondrial Uncoupling, Fatty-Acid β-Oxidation, Adipogenesis, Insulin Sensitivity, Adiponectin, Visceral Fat.

Acts on 8 of these pathways: AMPK, Weight & Body Fat, Incretin, Satiety, Insulin Sensitivity, Fasting Insulin, Adiponectin, Gastric Emptying.

Acts on 6 of these pathways: AMPK, Weight & Body Fat, Insulin Sensitivity, Fasting Insulin, Adiponectin, Leptin Signaling.

Acts on 6 of these pathways: Weight & Body Fat, Fatty-Acid β-Oxidation, Hormone-Sensitive Lipase, Lipolysis, Protein Kinase A, Visceral Fat.