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?
The body mainly uses serum triglycerides for energy. After eating, fats from food are absorbed in the intestines, converted into triglycerides, and transported through the blood by lipoproteins. Chylomicrons, large lipoproteins, carry dietary fats and cholesterol from the intestines to the liver, muscles, and other tissues, while Very Low-Density Lipoprotein (VLDL) transports triglycerides from the liver to the body’s cells. Any excess triglycerides are stored in fat cells for future use.
When the body needs energy—like between meals, during exercise, or fasting—hormones signal the release of 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 – this includes a coctail of enzymes and hormornes: Lipoprotein Lipase (LPL), Hormone-Sensitive Lipase (HSL), Glucagon, and Epinephrine
Normies: How Insulin Works on Triglycerides
In a normal human, insulin, Lipoprotein Lipase (LPL), Hormone-Sensitive Lipase (HSL), Glucagon, and Epinephrine work together to regulate fat storage and energy use in the body.
1. Insulin (Energy Storage & Fat Formation)
- Released after eating when blood sugar is high.
- Activates LPL, which helps store triglycerides in fat cells.
- Deactivates HSL, preventing the breakdown of stored fat.
- Suppresses glucagon to stop glucose release from the liver.
2. LPL (Fat Storage)
- Activated by insulin to store triglycerides in fat cells.
- Helps move fats from the bloodstream into tissues for storage.
3. HSL (Fat Breakdown)
- Turned off by insulin to prevent fat breakdown when energy is abundant.
- Activated by glucagon and epinephrine when energy is needed, breaking down stored fat into free fatty acids (FFAs) for fuel.
4. Glucagon (Energy Release from Stored Glucose & Fat)
- Released when blood sugar is low (fasting, exercise, etc).
- Signals the liver to break down glycogen and release glucose.
- Activates HSL to break down stored fat when needed.
- Opposed by insulin, which suppresses glucagon release when glucose is high.
5. Epinephrine (Quick Energy During Stress & Activity)
- Released during stress, exercise, or fasting.
- Signals fat and muscle cells to break down stored energy.
- Activates HSL, promoting fat breakdown for energy.
- Works alongside glucagon to release stored glucose and fat.
How They Work Together
- After Eating: Insulin is high → LPL stores fat, HSL is turned off, glucagon & epinephrine are suppressed.
- During Fasting/Exercise: Insulin is low → Glucagon and epinephrine rise → HSL breaks down stored fat → Fatty acids & ketones are used for energy.
This balance ensures the body efficiently stores energy when food is available and burns fat when needed.
Metabolic Syndrome Insulin Breaks the Lipolysis Process
In metabolic syndrome, the normal balance between insulin, LPL, HSL, glucagon, and epinephrine is disrupted, leading to insulin resistance, fat accumulation, and inefficient energy use. Here’s how the process breaks down:
1. Insulin Resistance Develops
- In healthy individuals, insulin helps store energy by activating LPL (to store fat) and deactivating HSL (to prevent fat breakdown).
- In metabolic syndrome, cells become resistant to insulin, meaning the body needs more insulin to achieve the same effects.
- The pancreas compensates by producing excess insulin (hyperinsulinemia) to regulate blood sugar.
2. Fat Storage Becomes Excessive
- LPL remains active, continuing to store fat in fat cells.
- Since insulin is high most of the time, HSL stays suppressed, meaning stored fat is not broken down efficiently for energy.
- This leads to increased fat accumulation, particularly in the abdomen (visceral fat).
3. Fat Breakdown is Impaired
- Normally, when insulin levels drop (such as during fasting or exercise), HSL activates to break down stored fat for energy.
- In insulin-resistant individuals, insulin levels remain chronically elevated, keeping HSL suppressed, so the body struggles to release stored fat.
- As a result, fat stays locked in fat cells, even when energy is needed.
4. Glucagon and Epinephrine Become Less Effective
- Since insulin is always high, glucagon’s ability to raise blood sugar and mobilize fat is weakened.
- Epinephrine’s fat-burning effects are also reduced, making it harder for the body to access stored energy during stress or exercise.
5. The Liver Produces Excess Glucose & Fat
- Despite high insulin levels, the liver still produces glucose because insulin resistance prevents normal glucose regulation.
- The liver also converts excess carbohydrates into triglycerides, worsening fat accumulation and contributing to high blood triglycerides (dyslipidemia).
6. The Cycle Worsens Over Time
- More fat is stored → More insulin is needed → Insulin resistance increases → Fat remains trapped in cells → The body relies more on glucose → Blood sugar levels rise → Risk of type 2 diabetes, fatty liver, and cardiovascular disease increases.
In short, metabolic syndrome makes the body produce too many triglycerides, unable to store them properly, and struggles to clear them from the blood, leading to high serum triglycerides.
Disclaimer: I had a hard time understanding insulin’s relationship with triglycerides and I think I did my best trying to explain the whole process. I’m not a medical expert. I’m a person with metabolic syndrome trying to understand what it all means.
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.
