Sunday, July 24, 2011

Type 2 Sugar Diabetes

The best article on the internet about diabetes:

It's the disease that's becoming more and more prevalent among westernized cultures. Diabetes, along with the obesity epidemic that's fueling it, is growing rampant and the numbers behind the illness are almost too large to wrap your mind around. According to the American Diabetes Association (ADA) 25.8 million people have diabetes in the United States. That's approximately 8.3% of the population. But that's not the disturbing part. The real kicker is another 79 million people in the U.S. are at risk for developing diabetes and are classified as having prediabetes

For the whole article

Here's more about IMCL:

Insulin resistance is common in obesity [10,11], as evidenced by low rates of whole-body glucose uptake during euglycemic-hyperinsulinemic clamping [12]. Weight loss has been shown to improve insulin-mediated glucose disposal by enhancing both oxidation and storage of glucose in skeletal muscle [13,14,15]. The mechanisms whereby weight loss, by diet or surgery, improves insulin resistance are incompletely understood. Recently, attention has focused on the content, localization, and composition of fat within skeletal muscle as determinants of insulin resistance. Several studies have reported an inverse relationship between insulin action and the fatty-acid composition of skeletal muscle phospholipids [16], muscle triglyceride levels [17,18,19,20], and saturated fatty acids in muscle triglycerides [21]. Less information is available on the localization, intracellular or interfibrillar, of lipids in human skeletal muscle and its specific impact on insulin action. Muscle attenuation on computed tomography scans, believed to reflect intramuscle lipid content, has been reported to be accentuated in obese women [22] and to be reciprocally related to insulin sensitivity [20]. Proton magnetic resonance spectroscopy has been validated against a chemical extraction method and used to establish a reciprocal relationship between intramyocellular lipid accumulation and insulin sensitivity in healthy individuals [23]. The accuracy of this approach in obese patients or obese patients with diabetes has not been established, however. By quantitative histochemistry, Phillips et al. [18] found an inverse relationship between intracellular lipids in the gastrocnemius of nondiabetic women and muscle glycogen synthase activity but not insulin sensitivity. In another ex vivo study using histochemistry, lipid accumulation was demonstrated within muscle fibers of the vastus lateralis in obese individuals [24].

The relation of intramyocellular fat depots to total body fat and their physiological regulation are not well known. In rats fed a high-fat diet, acute dietary lipid withdrawal is associated with an improvement of muscle insulin resistance [25]. Likewise, reducing tissue lipid availability in rats by peroxisome proliferator–activated receptor- agonism has been reported to enhance insulin sensitivity [26]. On these grounds, it has been hypothesized that selective depletion of intracellular fat depots in skeletal muscle is the key metabolic change that leads to reversal of insulin resistance independent of fat mass (FM) loss

In this video link below, Dr Furhman explains how his article was denied for publication in a diabetes magazine:

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