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Lipolysis is the metabolic process through which triacylglycerols (TAGs) break down via hydrolysis into their constituent molecules: glycerol and free fatty acids (FFAs). Fat storage in the body is through adipose TAGs and is utilized for heat, energy, and insulation. The body uses fat stores as its main source of energy during starvation, conserving protein. Overall, fats are quantitatively the most important fuel in the body, and the length of time that a person can survive without food depends mainly on the amount of fat stored in the adipose tissue. Thus, lipolysis is especially important in the fasting state of metabolism when blood glucose levels have decreased. However, it also occurs under non-stimulated (basal conditions).[1] The glycerol produced by lipolysis is a source of carbon for gluconeogenesis in the liver. FFAs are transported in the blood bound to albumin and are either oxidized in tissues by a process called beta-oxidation or converted to ketone bodies. The byproducts of beta-oxidation, ATP, and NADH, promote gluconeogenesis. FFAs convert to ketone bodies in the liver, which serves as an energy source for the brain, thus decreasing further consumption of already depleted blood glucose. FFAs are utilized throughout the body for energy production or biosynthetic pathways except in white adipose tissue (WAT) where they are stored. In a metabolic "fasting" state, when the body is deprived of nutrients, WAT releases FFAs and glycerol to supply non-adipose tissues.[2] The major enzymes participating in lipolysis constitute adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), and monoglyceride lipase (MGL).

Neutral lipid storage disease with myopathy (NLSDM) – a rare inherited disorder arising from mutations in the ATGL gene, which results in systemic TAG accumulation, myopathy, cardiac abnormalities, and hepatomegaly.[6] Chanarin-Dorfman syndrome or NLSD with ichthyosis (NLSD-I) results from mutations in CGI-58, the activator of ATGL. They also exhibit systemic TAG accumulation, mild myopathy, and hepatomegaly but also present with ichthyosis, which is a skin disorder characterized by dry, thickened, scaly skin.[6] Familial partial lipodystrophy (FPLD) type 4 is associated with a mutation in the PLIN1 gene coding for perilipin 1. It is characterized phenotypically by loss of subcutaneous fat from the extremities. Histologically, the six patients with this mutation have small adipocytes with increased macrophage infiltration and abundant fibrosis.[7] Familial partial lipodystrophy (FPLD) type 6 occurs due to a mutation in the LIPE gene coding for hormone-sensitive lipase. It is characterized by abnormal subcutaneous fat distribution, and thus the complications commonly associated with it it. These include dysregulated lipolysis, insulin resistance, diabetes mellitus, increased fat storage in bodily organs, and dyslipidemia; others may even develop muscular dystrophy as indicated by elevated serum creatine phosphokinase.[8] There are many disorders of fat metabolism that present with serious and specific characteristics but are not discussed here as they are beyond the scope of lipolysis, specifically. These include, but are not limited to, fatty acid oxidation disorders (FAODs) such as MCAD deficiency or primary carnitine deficiency and peroxisomal disorders such as Zellweger syndrome and adrenoleukodystrophy.