[Nutrition_Reports] Fructose metabolism by the brain increases food intake and obesity

[Guest guest]

It looks like the bottom line is that eating or drinking too much sweetened

foods and beverages makes you fat! Wow! Amazing fact. They seem to be

villainizing high fructose corn sweetener, but briefly stick in " and table

sugar " in parentheses. The hype about HFCS may be just that. If we switch back

to sucrose, I don't think anything would change. I remember as a little boy

drinking Coke in six ounce bottles after playing hard all morning outside on the

farm. What changed was the serving sizes and lack of activity.

W. Rowell, RD, LN

Montana State Hospital, Warm Spring, MT

Consultant Dietitian, Long Term Care

Certified LEAP Therapist

________________________________

From: Nutrition_Reports

[mailto:Nutrition_Reports ] On Behalf Of ne Holden

Sent: Thursday, March 26, 2009 7:04 AM

To: Nutrition_Reports

Subject: [Nutrition_Reports] Fructose metabolism by the brain increases food

intake and obesity

Public release date: 25-Mar-2009

http://www.eurekalert.org/pub_releases/2009-03/e-fmb032409.php

Contact: Adriaan Klinkenberg

f.klinkenberg@...<mailto:f.klinkenberg%40elsevier.com>

31-204-852-456

Elsevier

Fructose metabolism by the brain increases food intake and obesity

Increase in consumption of high fructose sweeteners raises concerns

Amsterdam, 25 March 2009 - The journal Biochemical and Biophysical

Research Communications (http://www.elsevier.com/locate/ybbrc) (BBRC),

published by Elsevier, will publish an important review this week

online, by M. Lane and colleagues at s Hopkins, building on

the suggested link between the consumption of fructose and increased

food intake, which may contribute to a high incidence of obesity and

Type 2 diabetes.

Over the past four decades life-styles have gravitated toward the

excessive consumption of 'high energy' foods and sedentary behavior that

has resulted in a high incidence of obesity and its pathological

consequences. This scenario has led to the increased occurrence of

insulin resistance and Type 2 diabetes. At present, approximately thirty

percent of adult Americans can be classified as obese. Moreover, these

changes now extend into the younger age group.

M. Lane and co-workers at The s Hopkins University School of

Medicine in Baltimore have now pulled together work, largely in their

laboratory (many papers beginning in 2000), dealing with the role of

malonyl-CoA in the signaling system in the brain (specifically the

hypothalamus) that has inputs into the higher brain centers that

determine feeding behavior, most notably appetite. Two papers in the

journal PNAS in 2007 and 2008 showed that glucose and fructose act quite

differently in the brain (hypothalamus) - glucose decreasing food intake

and fructose increasing food intake. Both of these sugars signal in the

brain through the malonyl-CoA signaling pathway and have inverse effects

on food intake.

Lane commented: " We feel that these findings may have particular

relevance to the massive increase in the use of high fructose sweeteners

(both high fructose corn syrup and table sugar) in virtually all

sweetened foods, most notably soft drinks. The per capita consumption of

these sweeteners in the USA is about 145 lbs/year and is probably much

higher in teenagers/youth that have a high level of consumption of soft

drinks. There is a large literature now that correlates, but does not

prove that a culprit in the rise of teenage obesity may be fructose. "

The fact that fructose metabolism by the brain increases food intake and

obesity risk raises health concerns in view of the large and increasing

per capita consumption of high fructose sweeteners, especially by youth.

###

Notes to Editors:

The article, appearing in Volume 382/1 (print edition: coverdate April

24) is available on ScienceDirect at

http://dx.doi.org/10.1016/j.bbrc.2009.02.145, copies of the full text

are available to members of the media by contacting the Elsevier press

office, newsroom@...<mailto:newsroom%40elsevier.com>.