Hormonal
Short-term surplus carbohydrate intake (50% excess for 5 days) significantly increases fasting hepatic glucose production (HGP) and serum insulin levels, creating a state of insulin resistance that suppresses lipolysis and shifts whole-body fuel selection toward carbohydrate oxidation and away from fat oxidation.
Eating significantly more carbohydrates than usual for a few days doesn't make you fat; it changes your metabolism to burn those carbs instead of fat. This happens because your liver produces more glucose and your insulin levels rise, which signals your body to stop breaking down fat stores. To manage this, be aware that high-carb meals will suppress fat burning for a period, regardless of total calories.
Fasting hepatic glucose production (HGP) varied by > 40% from deficient to surplus CHO diets... Increased HGP on surplus CHO occurred despite significantly higher serum insulin concentrations... Lipolysis correlated inversely with CHO intake as did the proportion of whole-body lipolytic flux oxidized... Whole-body CHO oxidation increased sixfold and fat oxidation decreased > 90% on surplus CHO diets.
Why this rating
Controlled metabolic ward study with stable isotope tracing in healthy subjects.
Source
Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection.
Jean‐Marc Schwarz et al. · Journal of Clinical Investigation · 1995
DOI 10.1172/jci118342
More from this paper
- Short-term carbohydrate deficiency (50% deficit for 5 days) reduces fasting hepatic glucose production (HGP) and improves the sensitivity of HGP to suppression by insulin, leading to increased fat oxidation.Good
- Fractional hepatic de novo lipogenesis (DNL) is a sensitive and specific biomarker for recent carbohydrate intake, increasing more than 10-fold on surplus carbohydrate diets and becoming unmeasurable on carbohydrate-deficient diets, even though absolute fat synthesis remains low.Good
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