Weight

cycling permanently elevates resting energy expenditure, causing extreme

metabolic stress that triggers compulsive caloric overconsumption.

Glut4

(Glucose Transporter 4).

Gut

bacteria produce high concentrations of butyrate and propionate, which directly

inhibit white adipose tissue lipolysis to decrease circulating free fatty acid

levels.

Gut

bacteria convert bile acids into secondary steroids that downregulate

uncoupling protein 1 (UCP1) expression, shunting energy toward muscle glycogen

storage.

Gut bacteria synthesise acetate and lactate,

which stimulate the browning (beiging) of white adipose tissue to elevate

thermogenesis and reduce overall adiposity.

Gut

bacteria deplete colonic lactate levels, forcing white adipocytes to undergo

hypertrophy and store excess lipids as monounsaturated triglycerides.

Thyroid-stimulating

hormone (TSH).

Glucagon-like

peptide-1 (GLP-1).

Brain-derived

neurotrophic factor (BDNF).

Feed

efficiency decreases, causing mice to store less fat despite increased total

food consumption.

Feed efficiency is reduced, meaning mice gain

body weight while consuming fewer total calories.

Feed

efficiency increases drastically, allowing mice to burn excess calories via

elevated brown fat activity.

Feed

efficiency remains unchanged, but total energy expenditure increases due to

heightened locomotor activity.

Live

birth rates increase from under 25% to over 40%, while pregnancy loss rates

decrease from approximately 40% to nearly 10%.