Insulin Resistance?

[Birdie]

Where I said sucrose, read table sugar/white sugar. When I say sugar, I can mean fruit or white or honey or etc, so I'm trying to say white sugar or table sugar for the emergency stuff, to be clear.

Also, of course, Ray never means to use fruit in coffee, so I assume that table sugar in coffee is always okay and not just for emergencies. I'm just thinking... But, still, in keeping with the spirit of things, I use honey in coffee whenever I can. For me that is in lattes, not brewed coffee, for taste reasons.

I get a lot of my sugar from orange juice and next comes fruit. It is easier to get more sugar from fruit in the summer. We're using canned fruit now. Canned with sugar and water only. Comes in glass. It helps to bake it, taste wise.

Yes I will try to maximize fruit as much as possible this winter. My plan is OJ, cooked/peeled apples, bananas in moderation, some fresh oranges if tolerated (stomach pain), and occasional frozen berries. What about pineapple juice? I always loved me some orange/pineapple juice combo.

Pineapple juice is high in serotonin...... If you do berries, be sure to strain out the seeds.. For the fresh oranges, you'll be sucking them? That's good for not getting the pulp that irritates the colon and maybe that's the problem with your tummy too.

 

[Eric Yim]

It seems to me that a peat based approach to eating puts you at risk for insulin resistance. Frequent meals, a lot of sugar, little vegetables/fiber. Just a thought. What do you guys think?

Intramyocellular Lipid and Insulin Resistance

"Insulin resistance (IR) is a common feature of the metabolic syndrome and an important factor in the cause of type 2 diabetes. There is abundant evidence that increased levels of plasma lipids, predominantly free fatty acids (FFAs) and triglycerides, are causally involved in IR (1). In the 1960s, Randle et al. (2) introduced the idea that FFAs interfere with insulin action in peripheral tissues. His group suggested a substrate competition between plasma glucose and FFAs as fuel for energy production, the “glucose fatty-acid cycle.” In humans, lipid infusion plus heparin, which acutely raises plasma FFA levels, inhibits insulin-stimulated glucose uptake in muscle, a finding consistent with increased peripheral IR. However, in a temporal sequence, this FFA-mediated impairment of insulin-stimulated glucose utilization developed with a delay of ∼3 h after starting the lipid infusion (3,4) and was accompanied by a fall rather than a rise in the muscle glucose-6-phosphate concentration (5) as expected by the original Randle hypothesis (6,7). In animal models, an increased IR was also observed after lipid infusion or high-fat feeding (8,9), which was accompanied by a rise of the triglyceride content in liver and skeletal muscle (10,11).

"On the basis of these findings and of the well-known fact that peripheral insulin sensitivity (IS) depends predominantly on glucose utilization in muscle tissue, recently not only the higher levels of circulating lipids but also the role of lipids accumulating within muscle cells received increasing attention. Currently, the ectopic deposition of fat in nonadipose tissue is considered an important aspect in the development of IR (1,7,12). Muscle triglycerides themselves do not seem to interfere directly with insulin action in the myocytes but rather to act through some other fatty acid-derived metabolite to impair insulin signaling. Long-chain fatty acyl-CoAs have been suggested as possible candidates (13–15)."