Are there any good reviews or specific chemicals to make adipocytes insulin resistant?
The best way is to give them glucolipotoxicity i.e., 500 micromolar palmitate and 35 mM glucose. You can give them for 6 hr or 12hr or even for 24 hr based upon your experiment. You can optimize it.
Glycemic control is like a religion. It is nice to see somebody actually thinking. My father was an engineer and he said the difference between him and me is a physician was engineers start at zero and work up and physicians have to start at the end of work backward. The zero point is actually an inherited capillary deficiency marked by a a thickened leaky basement membrane. The capillaries leak in enclosed spaces such as the pancreas, back of the retina in the nephron where leakage causes strangulation and a slow death of those cells. All that is seen after that is secondary to those injuries.
I believe there is a third type of diabetes, which I'm calling type III, that involves over eating, then fiddling with the hypothalamic fuel center, producing increased insulin in order to deal with the high-fat loads, and a subsequent compensatory signal to the liver to reduce sensitivity to insulin basically I think in order to prevent hypoglycemia during the time of the elevated insulin levels helping to store excess fat load. This is why "diabetics" will resume normal glucose is with a little bit of weight loss "Makes the diabetes go away. What is going away is elevated blood sugar a surrogate not the disease of capillaries. The high glucose level from not having enough insulin activated at the receptor level due to hypothalamic suppression is a protective mechanism not a pathological one. People with elevated and son levels are the cause of the diabetic worldwide epidemic based on the World Health Organization criteria of 126. this is scientifically illogical. To make the diagnosis of diabetes like any other disease there needs to be clinical correlates otherwise the diagnosis become simply a Surrogate lab test and over identifies millions of people which of course will need pharmacological treatment but who will never develop true vascular diabetes. Giving insulin to my T3 folks with "insulin resistance" and already high insulin levels is negligent
Thank all because of many helpful answers. But from my point, if the circulation of FFAs increases rapidly, that might give a relevance to insulin resistance, am I right?
So is that mean if I increase the proportion of my adipocytes, how can I detect the IR in my skeletal muscle?
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