Posted: Mar 09, 2011 4:08 am
Elena wrote:This is incorrect. The evidence is rather strong. An experimental model of insulin resistance and hyperinsulinemia induced precisely by a (low-fat) high sugar diet can be found here: http://jap.physiology.org/content/84/4/1311.full
From that paper,
Barnard et al wrote:
This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats.
and, later on:
Barnard et al wrote:
The results of this study clearly indicate that insulin resistance/hyperinsulinemia precedes the other characteristics of the metabolic syndrome. Furthermore, the data demonstrate that obesity is not the cause of insulin resistance/hyperinsulinemia, rather an HFS diet is the true underlying factor. Recent studies by Barnard et al. (2-4) have documented that diet appears to be a major factor in the metabolic syndrome and have shown that the syndrome can be induced in rats by feeding an HFS diet similar to the typical US diet and can be controlled in humans by feeding an LFCC diet combined with aerobic exercise.
The high fat, high sugar diet was compared to a low fat, complex carbohydrate diet. Sugar may increase insulin resistance but the study you linked doesn't demonstrate it because there is no control for a high fat, low sugar diet.
Shulman et al propose a method to decrease fat-mediated insulin resistance in the linked paper.
I'm not current in the field, so I apologise if my research is out of date. I've only re-familiarised myself via a relatively quick skim of the literature that popped up articles like:
Overnight lowering of free fatty acids with Acipimox improves insulin resistance and glucose tolerance in obese diabetic and nondiabetic subjects - which seems to indicate that blood FFA composition is quite important in insulin resistance.
Incorrect, re: both the short and the long term. In the short term, dietary glucose raises blood glucose and immediately triggers insulin secretion. In fact, the concentration of insulin parallels that of glucose.
I didn't deny that at all, but was specifically referring to the proposition by Taubes that high sugar intake increases long-term basal levels of insulin.
The study you quote does not control for the intake of fats but is more aimed at the question of dietary fibre vs sugar intake. While that is worthwhile, it is important to mention that whole grain foods are generally low in fat too.
Sorry, in the abstract you linked there is no support for your dismissal of the role of dietary sugar in insulin resistance. (And, it's a study on diabetics -not healthy people).
How so?
From the article:
Emphasis mine.
Furthermore, we have now increasing evidence that the adipose tissue not only produces free fatty acids that contribute to insulin resistance, but also acts as a relevant endocrine organ producing mediators (adipokines) that can modulate insulin signalling
Most studies on insulin resistance (the mechanism referred to indirectly by Taubes) are carried out in diabetic or pre-diabetic patients. This is because insulin resistance is one of the major risk factors for that disease.