Lipolysis
Lipolysis is the release of fatty acids from stored fat. Hormones and energy status control the rate.
Mechanism
[edit]Nearly all stored fat sits as triglyceride, three fatty acids on a glycerol backbone. Three enzymes strip it in sequence, ATGL, hormone-sensitive lipase (HSL), and monoacylglycerol lipase, releasing free fatty acids and glycerol into blood. HSL drives most of the rate above baseline. Adrenaline, noradrenaline, glucagon, growth hormone, and cortisol turn it up; insulin is the main brake.[1]
Why aggressive lipolysis backfires
[edit]Chronic exposure of pancreatic beta cells to elevated plasma free fatty acids impairs glucose-induced insulin secretion. Estrogen (probably via growth hormone) increases free fatty acid release, and adrenaline, elevated in hypothyroidism, increases release from storage; free fatty acids impair mitochondrial energy production.[2] The same elevated free fatty acid state shows up in obesity, type 2 diabetes, and insulin resistance; it is one of the few things that is both raised in obese people and produces insulin resistance when raised experimentally, and reduces it when lowered.[1]
This isn't limited to disease. A study measuring whole-body lipolysis directly with tracers found glycerol release running 48% higher in cachectic patients, with or without cancer, than in normal-weight volunteers, and no difference between the cancer and non-cancer cachectic groups, evidence that impaired nutritional status itself drives the rise, not the tumor.[3] Low-carbohydrate dieting, fasting, hard exercise, poor sleep, and psychological stress all raise free fatty acids through the same hormone set, HSL turned up by adrenaline or cortisol, insulin turned down, so the same pattern that marks starvation shows up any time one of those is chronic.
Constant fasting, low-carbohydrate dieting, and stimulant-driven fat release are not recovery tools; they push free fatty acids up the same way undernutrition does, feeding insulin resistance and slowing metabolism rather than lowering the problem load. Steady blood sugar and lower stress load bring FFA back down, not more lipolysis.
Persistent pollutant release during fat loss
[edit]Fat tissue is the body's main storage compartment for lipophilic persistent organic pollutants (POPs), industrial chemicals such as PCBs, dioxins, and organochlorine pesticides that resist breakdown and accumulate over a lifetime. Storing them in fat protects other organs from direct exposure, but the store is not inert. Fat continually releases small amounts of accumulated POPs back into blood, and release rises further during active fat loss, making body fat a standing source of internal exposure to these compounds rather than a permanent sink.[4]
See also
[edit]References
[edit]- ↑ 1.0 1.1 Althaher AR. "An overview of hormone-sensitive lipase (HSL)," ScientificWorldJournal. 2022;2022:2314658. PMID 36530555.
- ↑ Ray Peat, "Diabetes, scleroderma, oils and hormones," raypeat.com.
- ↑ Klein S, Wolfe RR. "Whole-body lipolysis and triglyceride-fatty acid cycling in cachectic patients with esophageal cancer," J Clin Invest. 1990;86(5):1403-1408. PMID 2243120.
- ↑ La Merrill M, Emond C, Kim MJ, et al. "Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants," Environ Health Perspect. 2013;121(2):162-169. PMID 23221922.