Skip to comments.Researchers Link Obesity and the Body's Production of Fructose
Posted on 09/11/2013 3:10:21 PM PDT by neverdem
Researchers at the University of Colorado School of Medicine reported today that the cause of obesity and insulin resistance may be tied to the fructose your body makes in addition to the fructose you eat.
In recent years the role of added sweeteners, such as high fructose corn syrup and table sugar (sucrose), has taken center stage as risk factors for obesity and insulin resistance. Numerous studies suggest that the risk from added sugars may be due to the fructose content.
But in the study published in the Sept. 10 edition of Nature Communications, the team led by researchers at the CU School of Medicine reports that fatty liver and insulin resistance may also result from fructose produced in the liver from non-fructose containing carbohydrates.
The study, whose first authors are Miguel Lanaspa, PhD, and Takuji Ishimoto, MD, reported that mice can convert glucose to fructose in the liver, and that this conversion was critical for driving the development of obesity and insulin resistance in mice fed glucose.
"Our data suggests that it is the fructose generated from glucose that is largely responsible for how carbohydrates cause fatty liver and insulin resistance," said Lanaspa.
Richard Johnson, MD, professor of medicine and chief of the division of renal diseases and hypertension at the School of Medicine and senior author of the paper, said: "Our studies provide an understanding for why high glycemic foods may increase the risk for obesity and insulin resistance. While some of the weight gain is driven by the caloric content and the effects of stimulating insulin, the ability of high glycemic foods to cause insulin resistance and fatty liver is due in part to the conversion of glucose to fructose inside the body...
(Excerpt) Read more at sciencedaily.com ...
The #1 cause of obesity is... COMPUTERS!
Dietary fructose linked to liver damage by gut bacteria mechanism: Animal data
“may also result from fructose produced in the liver from non-fructose containing carbohydrates.”
Oh oh! Beer?
So. Wonder how much of the differential endogenous production of fructose is epigenetically determined.
Well, that and TV!
I used to think HFCS-55 was close enough to sucrose too, but the theoretical HFCS-55 has only 42 % glucose, i.e. it's almost four parts fructose to three parts glucose. 56/42 = 4/3. What they found in actual samples can be up to about 2:1.
hfcs hplc is sufficient to retrieve the citation at PubMed.
FReepmail me if you want on or off the diabetes ping list.
Corn growers and processors are not pleased.
But, the result of HFCS use in so many products, in addition to corn’s use in so many processed foods, is visually evident. Unavoidably evident.
I ask this as I gaze at my navel in the midst of my very well padded midsection.
I actually eat less than just about any other female in my age group too. (epi)genetics really stink.
And let’s remember corn allergy-related behavioral issues, as well here.
That Atkins was on to something, wasn’t he...
E A T L E S S
The trick isn’t to force yourself to eat less, it’s to eat what satiates you. When you do, you’ll eat less without hunger and without thought.
Thanks for the link.