Insulin…it’s not just a pill for treating diabetes.

Insulin is a hormone that has many effects on metabolic and cellular processes in the tissues and organs of the body. Insulin’s main action is to stimulate the uptake of glucose (from meals) into skeletal muscle and the heart and to inhibit the production of glucose and triglycerides in the liver. Insulin regulates the metabolism of carbohydrates, proteins, and fats after a meal and promotes cell growth.

If we consume too many calories, the excess glucose is converted by the liver to free fatty acids. These free fatty acids (FFAs) are transported as triglycerides in lipoproteins called very low-density lipoproteins (VLDLs), through the blood, and deposited in our adipose (fat) tissue.

An excess of free fatty acids has been associated with insulin resistance because it is believed to impair the insulin-signaling pathway. While insulin sensitivity is the ability of insulin to signal body tissues to take up and utilize glucose and inhibit FFA formation in the liver, insulin resistance results when this sensitivity is impaired and normal levels of insulin in the body no longer signal the absorption of glucose into the tissues. The results is an excessive level of insulin the blood trying to maintain normal blood glucose levels.

One of the main consequences of excess food intake leading to chronic insulin resistance is inflammation, which is the body’s natural defense mechanism when it encounters toxins. Besides excess calories, a large part of this inflammation is thought to be due to the intake of certain types of fats in our diet; in particular omega-6 fatty acids and saturated fats (especially arachidonic acid and palmitic acid). These fats are considered pro-inflammatory because they lead to insulin resistance. Other fats, such as omega-3 fatty acids, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are considered anti-inflammatory, as they can decrease insulin resistance.

Intake of saturated fats (palmitic acid in particular) or excess calories in general can lead to a decrease in satiety cues, giving us the feeling of fullness after a meal) coming from the hypothalamus region of the brain, which then leads to an increase in hunger and intake of more calories. The hypothalamus has binding proteins for omega-3 fatty acids such as EPA and DHA, meaning intake of these fats can decrease inflammation. The hypothalamus also has receptors for the omega-9 fatty acid oleic acid. When oleic acid is consumed, it binds to receptors in the hypothalamus and leads to satiety, which normally triggers us to stop ingesting more calories.

The best place for the body to store excess fat calories is the adipose (fat) tissue which can expand and store excess intake as triglycerides. Fat cells, however, do not have a limited capacity to expand, and once these fat cells have expanded to their limit, they essentially become starved of oxygen, leading to inflammation and later insulin resistance. This in turn can lead to FFA release from fat cells to the circulation and uptake by other organs such as the liver or skeletal muscle which are not able to safely store large amounts of fat. This in turn leads to insulin resistance in these organs.

The build-up of FFAs in the liver is known as non-alcoholic fatty liver disease (NAFLD). Approximately 30% of Americans and 90% of obese individuals with type 2 diabetes have NAFLD. Someone may be obese from excess intake and have no insulin resistance if the fat cells have not yet reached the point of over-expansion. Nonetheless, insulin resistance in the liver is related to FFAs in the liver, not in visceral fat, the fat around our abdomen. This is thought to explain why some normal weight individuals are found to have insulin resistance in the liver. Even in normal weight individuals, this insulin resistance can lead to increased levels of VLDLs (TGs) and decreased levels of HDL cholesterol, the “good” cholesterol which carries cholesterol from the body to be processed in the liver and then flushed out of the body.

Insulin resistance in the adipose tissue leads to excess fat being released into the bloodstream and taken up by the liver and skeletal muscle tissue which are not able to handle this excess fat. As a result, normal metabolic functions are inhibited. This leads to the development of such chronic conditions associated with insulin resistance, including type 2 diabetes, heart disease, and polycystic ovary syndrome.

As we can see, the types and amounts of fats in our diet have a very important role in the development or suppression of insulin resistance. So, how do we translate that to nutrition advise? What foods should we eat, and which should we avoid so that we steer clear of these inflammatory fats which can lead to overindulgence and insulin resistance?

Foods highest in inflammatory saturated fatty acids are:

1. Palm oil
2. Vegetable shortening and lard
3. Butter, both salted and unsalted
4. Pork
5. Beef
6. Rice bran oil
7. Egg yolks
8. Chicken
9. Cream from milk fat
10. Potato chips (often made with palm oil and other inflammatory oils)

Fish such as salmon, trout, and tuna are high in omega-3 fatty acids. For those who have a fish allergy or choose to avoid fish, many plant foods are also excellent sources of omega-3 fatty acids.

Plant foods highest in anti-inflammatory omega-3 fatty acids and polyunsaturated fat from oleic acid are:

1. Chia seeds
2. Hemp seeds
3. Walnuts
4. Flaxseeds
5. Flax oil
6. Avocados
7. Cashews
8. Almonds
9. Pistachios
10. Hazelnuts

We now know that not all fats are equal and the fats we choose to eat can have significant consequences to our body functions and risk for developing chronic conditions such as diabetes and heart disease.

Check out some of my recipe videos featuring these foods rich in omega-3s and oleic acid.

References:

1. Sears B, Perry M. The role of fatty acids in insulin resistance. Lipids in Health and Disease. 2015. 14:121
2. Jellinger P. Metabolic Consequences of Hyperglycemia and Insulin Resistance. Clinical Cornerstone. Glucose Dysregulation. 2007. 8(7):S30-S42.
3. Wilcox G. Insulin and Insulin Resistance. Clinical Biochemist Review. 2005. 26:19-39.
4. What’s In the Foods You Eat. US Department of Agriculture. Agricultural Research Service. Accessed from https://reedir.arsnet.usda.gov/codesearchwebapp/(S(5ltc3grjhrnhogdz5boylvni))/CodeSearch.aspxon 07/19/2020.