C15:0 or just milk fat?

Healthy Aging

Separating the wheat from the chaff

In this series, we are catching up on the latest peer-reviewed C15:0 science that has been published during 2023.

This week, let’s talk about another new study published in Nutrients, which sought to determine which of the following provided the most benefits: C15:0 (pentadecanoic acid), C17:0 (heptadecanoic acid), or milk fat.

What was the reason for this study?

Well, numerous previous studies have shown that people with higher levels of odd-chain saturated fatty acids (aka C15:0 and C17:0) have a lower risk of developing type 2 diabetes, insulin resistance, and nonalcoholic fatty liver disease (also called NAFLD). Because our main sources of C15:0 and C17:0 are dairy products, these studies couldn’t tell us which of the following may be causing these health protective benefits: C15:0, C17:0, or dairy fat?

Well, that’s interesting. How did this study compare C15:0, C17:0 and milk fat?

In the first part of their study, Bishop et al. fed mice a high-fat diet known to cause insulin resistance, type 2 diabetes, and NAFLD. They then supplemented mice with C17:0 or milk fat for five months to see if either helped to 1) improve insulin sensitivity or 2) reduce the severity of liver disease.

We presume they didn’t include C15:0 because prior studies had already shown that C15:0 supplementation lowered inflammation, glucose, cholesterol, body weight gain, and the severity of liver disease in models of type 2 diabetes and NAFLD.

In the second part of their study, Bishop et al. treated diseased liver cells with either C15:0 or C17:0 to evaluate their effects on genes relevant to liver inflammation and insulin sensitivity.

Here’s what they found.

In the mouse study, C17:0 had no effects on body weight, cholesterol, glucose, insulin, liver fat accumulation, or liver gene activation compared to non-supplemented controls. So, nothing exciting there.

In contrast, milk-fat-fed mice had higher blood cholesterol, higher blood glucose, and larger liver fat droplets. Milk-fat-fed mice also had livers with upregulated genes relevant to higher inflammation and fibrosis (aka scarring). So, milk fat made mice worse.

In the liver cell studies, Bishop et al. showed that cells treated with C15:0 had positive insulin-sensitizing and anti-inflammatory responses. While C17:0 did not have this insulin-sensitizing effect, it did have anti-inflammatory effects similar to C15:0.

Interestingly, Bishop et al. also showed that C16:0 – which is present in high levels in milk fat – was pro-inflammatory and toxic to liver cells. This likely explains why milk fat was found to be harmful in the mouse study.