FAT DIET DETERMINANTS INSULIN RESISTANCE

Fat Diet Determinants Insulin Resistance

Fat Diet Determinants Insulin Resistance

Introduction

One can speculate, theorize and philosophize publicity nauseam why a certain percentage of humanity is overweight, and why another percentage is not, (Keijzers, 2002) regardless of both assemblies allegedly spending the identical number of calories and next the identical workout program.  An approximated 50 billion heaviness decrease dollars are expended every year to reimburse for the vague difference. Is it all genetic?

 

Hypothesis

     A high fat diet determinants insulin resistance. Insulin opposition has become an epidemiological difficulty for society.

 

Does a high fat diet origin insulin opposition without heaviness gain?

The main findings of the first phase of this study that feeding rats a high-fat diet leads to an increase in mitochondria and as a muscle to oxidize fat at the same time with the development of muscle insulin resistance. It was hypothesized that skeletal muscle insulin resistance mediated by mitochondrial failure, which limits fat oxidation and leads to accumulation of intramyocellular lipids. This concept is based on finding that the muscle insulin-resistant individuals usually contain ˜ 30% less mitochondria than insulin-sensitive control group (3-7). This phenomenon is also known as mitochondrial dysfunction, although the detailed assessment provided evidence that all other normal functioning of mitochondria. These findings seem incompatible with the notion that muscle insulin resistance mediated by mitochondrial disease.

Our findings that high-fat diets cause an increase in PGC-1a protein, the spectrum of mitochondrial proteins, fats, and oxidative capacity in skeletal muscle of rats differ markedly from those of a recent study that feeding mice a high fat diet for 3 WK reported decrease in muscle mRNA levels of PGC-1a and mitochondrial respiratory chain constituents by ˜ 90% and PGC-1a and cytochrome levels of protein C by ˜ 40%. Nevertheless, a number of earlier studies provided evidence that high-fat diets lead to an increase in mitochondrial enzymes in muscle, and we have shown that a significant increase in FFA cause an increase in mitochondrial biogenesis. In addition, Turner et al. recently reported that, as in the present study, feeding rats a high-fat diet resulted in an increase in mitochondrial enzyme activity, mitochondrial respiratory chain subunit levels of protein, fat and the potential for oxidation in skeletal muscle. Further evidence that fatty acids stimulate mitochondrial biogenesis comes from the finding that lowering of serum FFA, giving acipimox to rats resulted in ˜ 30% decrease in mRNA content of mitochondrial proteins and that overexpression of lipoprotein lipase in muscle leads to a significant increase in mitochondria (Solinas, 2007).

It is surprising that mitochondrial deficiency causes insulin resistance, the concept was so widely accepted, because it seems untenable in the context of what is known about the potential of skeletal muscle for oxidative metabolism. The mechanism by which 30% decrease in muscle mitochondria, it was suggested to induce insulin resistance of muscle disorders in the capacity for fat oxidation, which leads to the accumulation of intramyocellular lipids. In fact, the rate of substrate oxidation in resting muscle is not defined / limited mitochondrial oxidative capacity, ...