Tuesday, May 24, 2011

Leptin and Fructose by Jerry Brainum

The Corn Refiners Association, consisting of various companies that manufacture high fructose corn syrup (HFCS), has issued a report concluding that HFCS is no different than table sugar, or sucrose. Numerous studies have attributed the current epidemic of obesity to inactivity, eating too much, and also increased intake of two particular food ingredients, HFCS and trans fats. The composition of HFCS at first does appear similar to natural sugars. Although it comes in varying concentrations, HFCS is a combination of glucose, the sugar that circulates in the blood, and fructose. Sucrose, or common table sugar, is also composed of glucose and fructose. So does that mean that the Corn Refiners are correct? Is HFCS not any different than ordinary sugar? Consider the results of a recent rat study. It is acknowledged that most people get fat from eating too much sugar and fat. Doing so leads to not only increased bodyfat, but also leptin resistance.Leptin is a protein released from fat cells, discovered in the late 90s, it was at first thought to be the cure for obesity. This was based on the observation that when given to obese rats, leptin caused the rodents to rapidly lose all excess bodyfat. But fat humans aren't rats. In those who are obese, leptin is produced normally, but the leptin signal to the brain that would normally turn off appetite isn't received. As a result, fat people have high leptin levels in their blood, but since the appitite centers in the brain don't receive the leptin signal, appitite is increased. This results in a perpetual cycle of overeating and even more bodyfat synthesis. As noted, the main cause of leptin resistence in humans is excess consumption of fat and sugar.
       The rat study consisted of feeding the rats two types of diets. The first diet consisted of a sugar-free, 30% fat diet. The other diet consisted of 40% high fructose and 40% fat. The diets were consumed for 134 days. The rats consuming the fructose diet showed severe leptin resistance, but those consuming the sugar-free diet showed normal leptin response. At the 65th day of the study, half the rats in the fructose group were switched to the sugar-free, high fat plan. Viola!, those rats who switched soon showed normal leptin response. This took only three days to happen. The switched rats also showed increased adiponectin levels that were depressed when they consumed fructose. Adiponectin is another fat cell protein that's linked to increased bodyfat oxidation and less insulin resistance. Based on these findings, the study authors concluded that fructose is the active ingredient that causes leptin resistance. Unlike sucrose, where the two sugars, glucose and fructose are bonded, in HFCS the sugars are not bonded, which means you get a rapid fructose effect. This translates into increased triglyceride (fat) formation in the liver, along with a rapidly induced leptin resistance that leads to gross overeating.

Shapiro,A, et al. Prevention and reversal of diet-induced leptin resistance with a sugar-free diet despite high fat content. Br J Nutr 2011: in press.

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