I often read in comments elsewhere that people don’t understand how the fat we eat affects blood glucose levels. Here’s a recent one I saw:
“I still can’t figure out HOW meat and fat are supposed to cause diabetes when it has a practically zero effect on your blood sugar.”
They talk about carbohydrates, but fat and protein, they say, have no effect … that you can eat as much fat, as much saturated fat, as you want and it won’t affect glucose levels or glucose uptake.
Truth be told, everything we eat affects glucose clearing in one way or another. The macronutrients … carbohydrates, fat, and protein … all contribute to glucose clearing in unique ways.
Regarding dietary fat, Ricardi et al., in their review…
Dietary Fat, Insulin Sensitivity And The Metabolic Syndrome, Clinical Nutrition, 2010
… Describe several mechanisms for how dietary fat impacts glucose uptake. I’ll highlight two of them.
1. “Consumption of energy-dense/high fat diets is strongly and positively associated with overweight that, in turn, deteriorates insulin sensitivity, particularly when the excess of body fat is located in abdominal region.”
That’s an indirect method. The middleman there is overweight. But what if you delete the middleman? What if you eat a high-fat, particularly high-saturated-fat diet but keep your weight within a healthful range? Can it still lead to insulin resistance? Yes. Studies have shown it can.
The composition of our cell membranes is determined, in part, by the amount and type of fat we eat. Saturated fat is less flexible than unsaturated fat, and will contribute to less flexible, or less ‘fluid’ cell membranes. (e.g. less saturated vegetable oils are more fluid at room temperature than more saturated butter and lard.), and:
2. “Given that insulin signaling and recruitment of GLUT4 to the cell membrane in skeletal muscle are largely membrane-associated events, a more fluid membrane might be expected to be associated with improved insulin sensitivity.”
Indeed, Ricardi cites studies, including intervention studies, that bear this out … the more saturated fat in the cell membrane (and the more saturated fat we eat), the more insulin resistant the cell. (GLUT4 is a glucose transporter or “door” for glucose to enter the cell.)
I’ll add a third mechanism that they don’t address but I’ve read about (e.g. Polyunsaturated Fatty Acids: From Diet To Binding To PPARs And Other Nuclear Receptors, Genes and Nutrition, 2006).
3. Fatty acids (FAs) themselves can affect the expression of genes. For example, FAs can bind to proteins in the nuclear membrane, acting as transcription factors. (A group of these transnuclear proteins are known as PPARs. Some of the best known PPAR ligands are the thiazolidiediones … a class into which the diabetes drugs Avandia and Actos fall.) By controlling gene expression, FAs can and do control many processes, from lipid storage (lipid synthesis) to lipid oxidation (lipid breakdown), which, taken together, affect insulin sensitivity.
1. Fat can affect body weight and body composition, which can affect insulin sensitivity.
2. Fat can make cell membranes more or less fluid, affecting insulin sensitivity.
3. Fatty acids can control how genes get expressed, affecting insulin sensitivity.
There must be something else working too, something more immediate, because when you give people with type 1 diabetes a high-fat meal and a low-fat meal, they need more insulin to cover the high-fat meal, even though both meals contain the same amount of carbohydrate and protein.
Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes, Diabetes Care, April 2013
I thought this was interesting, from Ricardi, about omega-3 (n-3):
“The n-3 very-long-chain polyunsaturated fatty acids characteristic of fish intake were weakly negatively associated with insulin sensitivity. This tends to confirm earlier findings that n-3 polyunsaturated fatty acid intake can impair insulin sensitivity.”
So, fish oil may contribute to insulin resistance as well. It’s already been shown to increase LDL cholesterol.1
There has been a lot of study in the area of diet and insulin resistance. That’s why comments like the one at the top of this post surprise me. There remain questions, but the body of evidence so far points to the notion that high-fat, especially high-saturated-fat diets increase insulin resistance, affect blood glucose levels, and contribute to the development of type 2 diabetes.
* “Insulin sensitivity” refers to how sensitive cells are to insulin, and how well cells take up glucose. If cells are insulin sensitive, that’s good. If cells are “insulin resistant”, that’s not good. It means cells are resistant to taking up glucose from the bloodstream, which can lead to high blood glucose and over time diabetes.
1 Effects Of Dietary Saturated, Monounsaturated And N-3 Fatty Acids On Fasting Lipoproteins, Ldl Size And Post-prandial Lipid Metabolism In Healthy Subjects, Atherosclerosis, 2003.