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A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans-4 Kim-Anne Le, David Faeh, Rodrigue Stettler, Michael Ith, Roland Kreis, Peter Vermathen, Chris Boesch, Eric Ravussin, and Luc Tappy ABSTRACT Background: High fructose consumption is suspected to be caus of intramyocellular lipids (IMCL)3,7,8). In humans, several stud ally linked to the epidemics of obesity and metabolic disorders. In es have addressed the chronic effects of fructose ingestion on lipid rodents, fructose leads to insulin resistance and ectopic lipid depo and carbohydrate metabolism, but many issues remain unresolved sition. In humans, the effects of fructose on insulin sensitivity remain A high fructose intake has clearly been shown to increase plasma debated, whereas its effect on ectopic lipids has never been invest riacylglycerol concentrations (9-11). In contrast, the effect of high whole-body insulin resistance with a concomitant accumulation fructose intakes on insulin sensitivity is still debated. As recently Objective: We assessed the effect of moderate fructose supplemen revewed, some authors have observed increased fasting glucose tation on insulin sensitivity (IS) and ectopic lipids in healthy male and insulin concentrations after high fructose consumption, volunteers (n 7). Design: IS, intrahepatocellular lipids (IHCL), and intramyocellular markers of insulin sensitivity (12). No study to date had ad lipids (IMCL) were measured before and after 1 and 4 wk of a high- dressed the effects of dietary fructose on ectopic lipids. fructose diet containing 1.5 g fructose . kg body wt·d ·Adipose In a previous study, we reported that a 6 d HFD induces dys issue IS was evaluated from nonesterified fatty acid suppression, he lipidemia as well as hepatic and adipose tissue insulin resistance patic IS from suppression of hepatic glucose output (6.6Hgluoe without altering whole-body insulin sensitivity (13). To further and muscle IS from the whole-body elucose disposal rate during a2-step delineate the metabolic consequences of a longer period of high hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured fructose consumption with a focus on insulin sensitivity, we by 'H magnetic resonance spectroscopy Results: Fructose caused significant (P0.05) increases in fasting amount of daily fructose consumption added to the diet corre plasma concentrations of triacylglycerol (36%), VIDL- sponded with the fructose content of 2 L of soda. triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, SUBJECTS AND METHODS IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk ofthe high-fructose diet (r -0.78, P

Explanation / Answer

High fructose intake is usually associated with obesity & metabolic disorders. However, its effect on lipid metabolism and insulin sensitivity (IS) has not been evaluated.

In the present study, the effect of fructose on ectopic lipid accumulation and IS was evaluated in 7 healthy volunteers. The volunteers were given a high fructose diet (1.5g fructose/ kgbodywt d) and IS, Intrahepatocellular lipids (IHCL) & Intramyocellular lipids (IMCL) were determined after 1 and 4 wks of administration. Adipose tissue IS, hepatic IS & muscle IS were found out from supression of non-esterified fatty acid, hepatic glucose output & body glucose disposal rate, respectively. 1H magnetic resonance spectroscopy was used to estimate IHCL & IMCL.

It was observed that, a moderate increase in fructose intake causes significant (P< 0.05) increase in plasma concentrations of triacylglycerol (36%), VLDL triacylglycerol (72%), leptin (48%), lactate (49%) & glucose concentration (5.5%). No significant change in IS, IHCL or IMCL was observed.

Hence, fructose intake alters lipid metabolism without causing ectopic lipid accumulation or insulin resistance in healthy humans.

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