At first glance, Fig 7A looks like a CIH believer's dream come true (apart from the words "High Fat Diet").
Obesity is caused by too much insulin. Game, Set and Match to insulin.
Not so fast! Let's take a look at the rest of Fig 7.
Revisiting the Current Model of Obesity and Type 2 Diabetes(A) The most widely accepted model of the pathogenesis of obesity and type 2 diabetes posits that a high-fat diet leads to obesity and insulin resistance (there is debate about the relative order and causality of these). In this widely held view, insulin resistance then leads to hyperinsulinemia, which is followed by β cell exhaustion, and then type 2 diabetes. The accepted model is incompatible with our results that put the insulin hypersecretion genetically upstream of obesity.(B) Our data support a model whereby insulin levels must be kept low to maintain energy expenditure in white adipose tissue via the expression of Ucp1. Our data do not address the order of subsequent events after obesity (outside the yellow box), such as insulin resistance and/or type 2 diabetes, since they were not observed in our studies. In other words, the effects of insulin gene dosage on obesity are independent of sustained changes in glucose homeostasis or insulin resistance.
↑ Peripheral Hyperinsulinemia → ↓ Uncoupling Proteins (WAT) → ↓ Energy Expenditure → ↑ Obesity.
Obesity is caused by a reduction in energy expenditure. Game, Set and Match to The Energy Balance Equation. It’s the Calories, Stupid. In the mice in this study, energy expenditure is strongly influenced by insulin levels. In humans, not a lot. In humans, insulin can act as a stimulant and as a sedative.
I'm not an insulin denier as is obvious from my other blog posts. I'm still controlling my carbohydrate intake.
I'm not a food reward denier and I've been using food reward principles to lose some more weight.
The above post will probably annoy some people. Before wasting your time writing a comment, please note my Moderation Policy.