Fructose, weight gain, and the insulin resistance syndrome
Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff and Peter J Havel

From the Department of Nutrition, University of California, Davis (SSE, JSS, and PJH); the US Department of Agriculture Western Human Nutrition Research Center, Davis, CA (NLK); and the Monell Chemical Senses Institute and the University of Pennsylvania, Philadelphia (KT).


This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic ß cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.

http://www.ajcn.org/cgi/content/abstract/76/5/911

Is that true?

Sheldon

Yes. That's the reason proponents of fructose claim it's a useful sweetener for diabetics. Fructose zooms into the liver so fast, there's little impact on blood sugar level or insulin.

Caveat: because it doesn't require insulin to enter the cell, fructose is more likely than glucose to cause the cells to become resistant to insulin. Also, the rate of glycolysation (or "caramelizing") of protein molecules, especially hemoglobin, is 15 times higher for fructose than glucose. Glycolysated hemoglobin, also known as HbA1c is now a standard test for diabetes.

I've posted more information about the dangers of fructose here.

Doreen

I don't understand why it would cause insulin resistance if it does not stimulate the production of insulin. I thought resistance comes from cells' overexposure to insulin.

Sheldon

Sheldon, do you have a copy of Protein Power Lifeplan? You might want to check out The Trouble With Fructose which is on pp 159 - 162. It's explained very well there.

Basically what happens is: the cells get used to not requiring insulin in order to admit fructose. Eventually, insulin receptors on the cells become less sensitive to the effect of insulin. What happens when glucose levels rise is that more insulin is required, since cells do require insulin to utilise glucose. Eventually insulin resistance develops.

Chronic fructose consumption is common, especially in children (most soft drinks and fruit drinks are sweetened with high-fructose syrup) .. and Type 2 diabetes is being diagnosed more and more in children. That's why Type 2 is no longer called Adult Onset diabetes

Another good article about the adverse metabolic effects of fructose was written by Nancy Appleton PhD. (author of "Lick the Sugar Habit) It's posted at Mercola's website http://www.mercola.com/2002/jan/5/fructose.htm

Hope this makes it a bit clearer,

Doreen