Researchers at the University of California, San Diego (UCSD) School of Medicine have reported in RxPG News that chronically high levels of insulin, as is found in many people with obesity and Type II diabetes, may block specific hormones that trigger energy release into the body. In other words, high insulin levels inhibit the use of body fat for energy in the body.
The researchers found in their studies that high levels of insulin can block stress hormones known as catecholamines, which normally cause the release of cellular energy. Adrenaline is the best known example of a catecholamine. For normal metabolism to occur, the body needs a balanced input of insulin and catecholamines. One of the actions of insulin --, the main energy storage hormone, is to block activation of the protein kinase A (PKA) enzyme. After a meal, insulin levels go up, and the body stores energy primarily as triglycerides, or fat, in adipose tissue to be used later. When energy is needed, catecholamine triggers activation of PKA, and energy is released. But in people with Type II diabetes, the hormonal balance has been thrown off, because the body continues to produce and store more triglyceride instead of breaking down the fat as released energy.
The findings provide additional understanding to the cause and effect occurring when insulin levels are chronically too high. We know that as insulin levels go up and the body loses the ability to effectively use it, so it makes more, bringing insulin levels even higher as the body struggles with what is called insulin resistence. Insulin resistence is a pre-cursor to Type II diabetes.
Overweight and obesity is seen in the vast majority of those with insulin resistence and Type II diabetes due to the chronic storage of fat in the body.
“If insulin levels get too high for too long a time – which happens in many patients with type II diabetes –the normal catecholamine signal that triggers fat breakdown and energy release can be drowned out. This can lead to excessive energy storage in the adipocyte,” said Hupfeld, assistant professor of Medicine in the UCSD Division of Endocrinology and Metabolism and a co-author of the paper. “This may be one reason why chronic obesity and Type II diabetes are often seen together.”
In lay terms, one gets fatter as their ability to effectively use insulin diminishes and their body makes more insulin, thus storing more energy as fat, in an effort to compensate for the insulin resistence. It really is a vicious cycle.
Now while the article continues to say that this data underscores the goal to bring down insulin levels - which I agree with - it fails to fully explore options other than using medications known as insulin sensitizers.
Too often, the medical community is dependent on the thinking that "managing" the problem with drugs is the short and long-term solution. While such an approach may be an effective short-term aid to bring things under control, it fails to address the need to reverse and eliminate the underlying cause of the chronic high insulin - poor diet.
We know from dozens of research studies that reducing carbohydrate, especially refined carbohydrates and sugars, stabilizes insulin levels and reduces the effects of insulin resistence. This is due, in part, to the lower levels of insulin required with less carbohydrate being metabolized to glucose, which in turn stimulates insulin, which in turn (especially when insulin resistence is present) leads to energy storage as fat. So, reducing carbohydrate intake is one effective dietary approach that can improve insulin sensitivity.
There are a number of controlled carbohydrate approaches available - everything from very low carbohydrate diets (Atkins) to moderate controlled carbohydrate diets (Zone) with a number of plans between the two ends of the spectrum of carbohydrate restriction (South Beach). No matter what approach you choose, one thing is important - this is not a short-term, temporary fix. It is something that you will need to follow for the long-term so choosing a plan you can live with for the long-term is key.