<p>Anti-Lipolysis Induced by Insulin in Diverse Pathophysiologic Conditions of Adipose Tissue</p>

Abstract

As an important energy reservoir, adipose tissue maintains lipid balance and regulates energy metabolism. When the body requires energy, adipocytes provide fatty acids to peripheral tissues through lipolysis. Insulin plays an important role in regulating normal fatty acid levels by inhibiting lipolysis. When the morphology of adipose tissue is abnormal, its microenvironment changes and the lipid metabolic balance is disrupted, which seriously impairs insulin sensitivity. As the most sensitive organ to respond to insulin, lipolysis levels in adipose tissue are affected by impaired insulin function, which results in serious metabolic diseases. However, the specific underlying mechanisms of this process have not yet been fully elucidated, and further study is required. The purpose of this review is to discuss the effects of adipose tissue on the anti-lipolysis process triggered by insulin under different conditions. In particular, the functional changes of this process respond to inconsonantly morphological changes of adipose tissue.

Nonalcoholic Fatty Liver Disease (NAFLD): Pathogenesis and Noninvasive Diagnosis

“…Lipolysis is a process of TG breakdown into FFAs by lipase enzymes to meet energy requirements. The activation of β-adrenergic leads to cyclic adenosine phosphate (cAMP) production [ 15 ]. These cAMPs bind to protein kinase A (PKA) and stimulate the phosphorylation of lipase enzymes [ 16 ].…”

“…This PNPLA2 lipase hydrolyzes the ester bond of TG into diacylglycerol (DAG), and hormone-sensitive lipase mediates the hydrolysis of DAG to monoacylglycerol (MAG). Following this, the monoglyceride lipase catalyzes the hydrolysis of MAG to glycerol and FFAs [ 15 ]. Usually, circulating FFAs are higher during fasting and decrease upon feeding due to insulin signaling, suppressing lipolysis.…”

“…However, in subjects with insulin resistance, higher lipolysis causes a more significant rise in circulating FFAs [ 9 ]. Mechanistically, upon insulin binding, insulin receptor substrate (IRS) is activated and phosphorylates phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB), also known as AKT (PI3K/AKT pathway), to initiate insulin-mediated effects [ 15 ]. One of the enzymes activated in this pathway is phosphodiesterase 3B (PDE3B), and this enzyme catalyzes the hydrolysis of cAMP to inhibit lipolysis.…”

Effect of the Aqueous Extract of Clerodendrum Thomsoniae Linn (Verbenaceae) Leaves on Type 2 Diabetic Wistar Rats Induced by the Macapos1 Type Diet and Dexamethasone

“…Concerning abdominal fat, AECT reduce the quantity in a dose-dependent manner with the highest reduction observed at 1250 mg/kg of AECT compared to the group of rats treated with metformin. In normal physiological state, insulin activates the lipolytic actions of the hormones on the deposit peripheral fat, hydrolyzing triglycerides and preventing storage of free fatty acids 39, 40 . In this experimental study, type 2 diabetic rats-showed significantly elevated quantity of abdominal fat.…”

A Review of the Epidemiology, Pathophysiology, and Efficacy of Anti-diabetic Drugs Used in the Treatment of Nonalcoholic Fatty Liver Disease

“…NAFLD is therefore usually regarded as a hepatic manifestation of the metabolic syndrome and diabetes. In healthy individuals, insulin inhibits hormone-sensitive lipase in adipose tissue, inhibiting triglyceride hydrolysis and free fatty acid (FFA) release [ 18 ]. In those with NAFLD, increased visceral adipocyte mass and the disinhibited activity of hormone-sensitive lipase in insulin resistance increase triglyceride hydrolysis, which increase plasma levels of FFAs, especially in the portal venous blood.…”