Diagram from the study showing: A high-fat diet leads to low oxygen in the fat cell, initiating an inflammatory response, resulting in insulin resistance and increased glucose output from the liver.

Since I was just talking about this (Mechanism By Which Dietary Fat Can Raise Blood Glucose And Insulin) I thought I’d post this study that appeared in my inbox this morning:

Increased Adipocyte O2 Consumption Triggers HIF-1α, Causing Inflammation And Insulin Resistance In Obesity, Cell, 5 June 2014

Here’s the press release:
The Connection Between Oxygen and Diabetes, A Lack Of O2 In Fat Cells Triggers Inflammation And Insulin Resistance In Obesity, University of California, San Diego School of Medicine, 5 June 2014

It’s known that dietary fat, both the quantity and the degree of saturation, promotes an inflammatory response. That inflammation promotes insulin resistance. These researchers say that fat-induced inflammation may be caused by increased oxygen consumption in mitochondria.

Researchers at the University of California, San Diego School of Medicine have, for the first time, described the sequence of early cellular responses to a high-fat diet, one that can result in obesity-induced insulin resistance and diabetes.

In today’s Cell paper, the scientists describe the earliest stages of [the development of systemic insulin resistance and diabetes], which begins even before obesity becomes manifest.

They observed that the abundant saturated fatty acids in the diet activated adenine nucleotide translocase 2 (ANT2) … [which] caused increased oxygen consumption, which meant less was available for the rest of the cell. The result was a relative state of hypoxia or inadequate oxygen supply, one that subsequently induced production of a protective transcription factor in fat cells called HIF-1alpha. In turn, HIF-1alpha triggered release of chemokines, proteins that signal cellular distress, launching the immune system’s inflammatory response. A sustained high-fat diet ensured that the process continued unabated, leading to obesity, chronic low-grade tissue inflammation and eventually, insulin resistance in the mice.