Treningsforum

Deltagerne fikk gå fra en isokalorisk diett (forbruk +-0) til 40% overskudd i to fem dager lange faser. En fase med høykarbo, og en fase med høyfett. Høykarbofasen ga signifikante forandringer i insulinsignalering i skjelettmuskulatur som er kompatible med høyere insulinfølsomhet. Høyfettfasen ga det motsatte.

Med andre ord: noen dager med overspising av karbo innimellom kan sannsynligvis være bra for deg.


Den isokaloriske dietten: 30% fett, 50% karbohydrater og 20% protein.

Høykarbofasen: 40% kalorioverskudd med 20% fett, 60% karbohydrater og 20% protein.

Høyfettfasen: 40% kalorioverskudd med 50% fett, 30% karbohydrater og 20% protein.



Early responses of insulin sensitivity to high-carbohydrate and high-fat overfeeding
Rebecca L Adochio , J WAYNE Leitner , Karen Gray , Boris Draznin  and Marc-Andre Cornier

Nutrition & Metabolism 2009, 6:37doi:10.1186/1743-7075-6-37

Published:   28 September 2009

Background
Early molecular changes of nutritionally-induced insulin resistance are still enigmatic. It is also unclear if acute overnutrition alone can alter insulin signaling in humans or if the macronutrient composition of the diet can modulate such effects.

Methods
To investigate the molecular correlates of metabolic adaptation to either high-carbohydrate (HC) or high-fat (HF) overfeeding, we conducted overfeeding studies in 21 healthy lean (BMI <25) individuals (10 women, 11 men), age 20-45, with normal glucose metabolism and no family history of diabetes. Subjects were studied first following a 5-day eucaloric (EC) diet (30% fat, 50% CHO, 20% protein) and then in a counter balanced manner after 5 days of 40% overfeeding of both a HC (20% fat, 60% CHO) diet and a HF (50% fat, 30% CHO) diet. At the end of each diet phase, in vivo insulin sensitivity was assessed using the hyperinsulinemic-euglycemic clamp technique. Ex vivo insulin action was measured from skeletal muscle tissue samples obtained 15 minutes after insulin infusion was initiated.

Results
Overall there was no change in whole-body insulin sensitivity as measured by glucose disposal rate (GDR, EC: 12.1 +/- 4.7; HC: 10.9 +/- 2.7; HF: 10.8 +/- 3.4). Assessment of skeletal muscle insulin signaling demonstrated increased tyrosine phosphorylation of IRS-1 (p<0.001) and increased IRS-1-associated phosphatidylinositol 3 (PI 3)-kinase activity (p<0.001) following HC overfeeding. In contrast, HF overfeeding increased skeletal muscle serine phosophorylation of IRS-1 (p<0.001) and increased total expression of p85alpha (P<0.001).

Conclusions
We conclude that acute bouts of overnutrition lead to changes at the cellular level before whole-body insulin sensitivity is altered. On a signaling level, HC overfeeding resulted in changes compatible with increased insulin sensitivity. In contrast, molecular changes in HF overfeeding were compatible with a reduced insulin sensitivity.




"We conclude that acute bouts of overnutrition lead to early changes at the
cellular level before whole-body insulin sensitivity is altered. Our lean healthy cohort
of subjects may be metabolically flexible and thus able to adapt to such changes in
their diet. High carbohydrate overfeeding induced mild elevations in insulinemia and
triglyceridemia, while still suppressing FFA, hepatic glucose production and
stimulating glucose disposal. On a signaling level, HC overfeeding induced changes
compatible with increased insulin sensitivity. In contrast, molecular changes in HF
overfeeding were compatible with a reduced insulin sensitivity, while in vivo insulin
sensitivity remained unchanged. More studies are needed to determine when these
early responses can no longer sustain normal whole-body insulin sensitivity and
which individuals may not be as capable of adapting to overnutrition and why. "


http://www.nutritionandmetabolism.com/content/pdf/1743-7075-6-37.pdf (http://www.nutritionandmetabolism.com/content/pdf/1743-7075-6-37.pdf)