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- January 6, 2009 |
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"Effect of Fructose Overfeeding and Fish Oil Administration on De Novo Lipogenesis and Insulin Sensitivity in Healthy Males"Dr. David Faeh (biography)
English - 2005-04-15 - 23 minutes
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Summary :
High fructose diets (Hfr) may stimulate hepatic de novo lipogenesis (DNL), and cause hypertriglyceridemia and insulin resistance in rodents. It can therefore be hypothesized that fructose-induced insulin resistance is secondary to alterations of hepatic and extra-hepatic lipid metabolism. Since fish oil supplementation (FO) is known to suppress lipogenic enzymes and to decrease TG, it may improve insulin sensitivity. We have thus studied the effect of Hfr and FO on DNL and VLDL-TG and their impact on insulin sensitivity. Seven normal men were studied on four occasions: after FO for 28 d (7.2 g/day), after a six-day Hfr (+ 25% total energy), after FO plus Hfr and control conditions. Following each condition, basal fractional hepatic DNL and hepatic glucose production (HGP) were evaluated using 1-13C sodium acetate and 6,6 2H2 glucose. Thereafter, a two-step euglycemic hyperinsulinemic clamp was performed to assess adipose, hepatic, and whole body insulin sensitivity. In basal conditions, Hfr significantly increased fasting glycemia (by 7%), TG (by 81%), DNL (by 490%) and HGP (by 14%, all p<0.05%). During hyperinsulinemia, Hfr was associated with an impaired suppression of adipose tissue lipolysis (p< 0.05) and with a trend toward a decreased suppression of HGP compared to control, but had no effect on whole body glucose disposal. FO significantly decreased Hfr-induced TG (by 37%, p<0.05) and tended to reduce DNL (by 21%, p=ns) but did not decrease HGP. In conclusion, Hfr impaired hepatic and adipose tissue insulin sensitivity and increased TG, but FO only improved hypertriglyceridemia.
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Animal and human studies relating to the metabolic effects of fructose overfeeding and fish oil supplementation
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