And we’re back with our journey in understanding Metabolic Syndrome, this time with its influence with Triglycerides. Let’s start with the basics.
What are Serum Triglycerides?
Serum triglycerides are a type of fat (lipid) found in your blood. They are the most common form of fat in the body and serve as a major source of energy. When you eat, your body converts excess calories into triglycerides and stores them in fat cells for later use. Between meals, hormones release triglycerides for energy.
The body uses serum triglycerides primarily as a source of energy. After eating, the body absorbs fats from food in the intestines. These fats are converted into triglycerides and transported in the blood via lipoproteins (such as chylomicrons and Very Low-Density Lipoprotein aka VLDL). Excess triglycerides are stored in fat cells (adipose tissue) for later use.
When energy is needed (such as between meals, during exercise, or fasting), hormones like glucagon and epinephrine signal the body to release stored triglycerides.
Here is where insulin comes in – it regulates the lipolysis process as it breaks down stored triglycerides into free fatty acids (FFA) and glycerol. It primarily inhibits lipolysis to promote fat storage and maintain energy balance.
Normies: How is Supposed to Insulin Work on Triglycerides
In a normal healthy person after eating the insulin levels are high. This activates Lipoprotein Lipase (LPL), an enzyme that helps store triglycerides in fat cells. Insulin also deactivates Hormone-Sensitive Lipase (HSL) which is responsible for breaking down stored fat.
Conversely, when insulin is low and in a normal human body, HSL is activated, breaking down stored triglycerides into free fatty acids and glycerol. FFAs are released into the bloodstream to be used as fuel by muscles, the liver, and other tissues. If glucose is scarce, the liver may convert fatty acids into ketones.
Metabolic Syndrome Insulin Breaks the Lipolysis Process
In humans with insulin resistance, insulin fails to effectively suppress lipolysis. This leads to excessive fatty acids in the blood, contributing to high triglycerides, fatty liver, and inflammation.
This is why elevated serum triglycerides are a hallmark of metabolic syndrome, and this elevation is closely linked to insulin resistance. In individuals with insulin resistance, these regulatory mechanisms are impaired.
Specifically, insulin resistance leads to increased lipolysis in adipose tissue, resulting in higher plasma FFA levels. These excess FFAs are transported to the liver, where they serve as substrates for triglyceride synthesis. Consequently, the liver secretes more VLDL particles, elevating serum triglyceride concentrations. Additionally, insulin resistance diminishes insulin’s ability to suppress hepatic glucose production and VLDL secretion, further contributing to hypertriglyceridemia.
Moreover, insulin resistance in muscle tissue reduces glucose uptake, leading to compensatory hyperinsulinemia. This state exacerbates hepatic lipid synthesis and VLDL production, perpetuating elevated triglyceride levels.
In summary, insulin resistance disrupts normal lipid metabolism by increasing free fatty acids release from fat stores and enhancing hepatic triglyceride production, culminating in elevated serum triglycerides characteristic of metabolic syndrome.
Resources
Grundy, Scott M, et al. “Definition of Metabolic Syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition.” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 24, no. 2, 2004, pp. e13-8. Accessed on 6 Feb 2025.
Grundy, Scott M . “Hypertriglyceridemia, Insulin Resistance, and the Metabolic Syndrome.” The American Journal of Cardiology, vol. 83, no. 9, May 1999, pp. 25–29. Accessed on 6 Feb 2025.
Savage, David B., et al. “Mechanisms of Insulin Resistance in Humans and Possible Links with Inflammation.” Hypertension, vol. 45, no. 5, May 2005, pp. 828–833. Accessed on 6 Feb 2025.