Insulin resistance and abdominal obesity typically occur simultaneously in metabolic syndrome, increasing the risk of several health complications.
Examine how insulin resistance and abdominal fat interact to understand their relationship:
Pancreatic insulin regulates blood sugar (glucose) levels. Insulin helps cells absorb glucose for energy when you eat, especially carbs. Insulin resistance develops when cells become insulin-resistant.
Obesity is the buildup of excess fat around the abdomen, particularly visceral fat. Visceral fat surrounds abdominal organs. Its metabolic activity releases chemicals that disrupt metabolism.
Free fatty acids enter the bloodstream from visceral fat in abdominal obesity. In peripheral tissues like muscles and liver, excess free fatty acids can interfere with insulin transmission, causing insulin resistance.
Adipokines are fat-cell signaling chemicals. Abdominal obesity causes adipokine imbalance and pro-inflammatory cytokines. Chronic inflammation causes insulin resistance.
Insulin usually suppresses fat breakdown, lipolysis. The release of fatty acids from adipose tissue increases in insulin-resistant conditions due to decreased inhibition. Fatty acids can worsen insulin resistance.
For personalized examinations and management of insulin resistance, abdominal obesity, and related health issues, consult a healthcare expert.