Originally posted by admin
Deels door een teveel aan glycogeen, dat kan niet anders.
De meeste mensen die te dik zijn halen meer dan 55% van hun kcal uit koolhydraten, wil je zeggen dat het enkel door die overige +-30% vetten is dat ze dik worden? Of enkel door de invloed die de koolhydraten hebben op de insuline agifte/gevoeligheid?
Nee niet specifiek door de insuline gevoeligheid. Glucose is de favoriete energiebron van (bijna) alles in het lichaam. Wanneer er veel glucose aanwezig is zal deze gebruikt worden voor de energie. Eet je daarbovenop ook nog vetten dan zullen deze niet als energie nodig zijn. Deze vetten zullen (grotendeels) opgeslagen worden.
Originally posted by admin
Een overschot aan koolhydraten moeten wel deels omgezet worden. Iedereen die lijd aan adipositas, zit in een abnormale situatie dus is het zoiezo mogelijk voor die groep.
Aangezien BB vaak hetzelfde aantal koolhydraten eten zie ik niet in wat het verschil uitmaakt.
Je kan wel degelijk dik/vetter worden door suikers die omzetten naar vet, daar twijfel ik geen seconde aan.
Dat mensen dik worden mede door suikers wordt grotendeels veroorzaakt door een andere oorzaak dan de echte omzettting van kh naar vet. Natuurlijk bestaat de conversie van kh naar vet en kan het voorkomen. Alleen wanneer deze al voorkomt dan zijn dit minieme hoeveelheden. Behalve wanneer je echt extreme hoeveelheden kh eet.
Maar ik zal nog een aantal samenvattingen posten dan kun je je eigen conclusie eruit trekken.
De novo lipogenesis in humans: metabolic and regulatory aspects.
Hellerstein MK.
Department of Nutritional Sciences, University of California at Berkeley, 94270-3104, USA.
The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute significantly to the whole-body energy economy.
It is concluded that DNL is not the pathway of first resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation.
Regulation of hepatic de novo lipogenesis in humans.
Hellerstein MK, Schwarz JM, Neese RA.
Department of Nutritional Sciences, University of California at Berkeley 94720-3104, USA.
The enzymatic pathway for synthesis of fatty acids from acetyl-coenzyme A, or de novo lipogenesis (DNL), is present in human liver and, to a lesser extent, in adipose tissue. Although the molecular and enzymatic regulation of the components for DNL are well characterized, the quantitative importance of the assembled pathway and its physiologic functions have remained uncertain. We review methods that have been used for measuring DNL in vivo, their limitations and the conclusions based on them. Two new methods for direct measurement of DNL in humans are discussed-mass isotopomer distribution analysis (MIDA), a mass spectrometric technique based on combinatorial probabilities, and 2H2O incorporation. Recent findings with these methods in a variety of dietary and hormonal settings are reviewed. In particular, we focus on the question of whether or not surplus carbohydrate energy is converted to fat by the liver in humans. A somewhat surprising model of the response to carbohydrate over-feeding emerges from these studies, with a number of implications for metabolic regulation in health and disease.
We close by speculating on potential functions of DNL in physiology and pathophysiology if storage of surplus carbohydrate energy is not an important function of DNL. The availability of techniques for quantifying DNL in vivo should make it possible to resolve these uncertainties regarding its functions and regulation in humans.
Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal.
Acheson KJ, Schutz Y, Bessard T, Ravussin E, Jequier E, Flatt JP.
In vivo lipogenesis and thermogenesis were studied for 24 h after ingestion of 500 g of carbohydrate (CHO) in subjects who had consumed either a high-fat, a mixed, or a high-CHO diet during the 3-6 days preceding the test. CHO oxidation and conversion to fat was significantly less in the high-fat diet group (222 +/- 5 g) than in the mixed (300 +/- 13 g) or high-CHO diet (331 +/- 7 g) groups, resulting in a greater glycogen storage in the high-fat (278 +/- 6 g) than in the other two groups (197 +/- 11 and 170 +/- 2 g). Net lipogenesis occurred sooner and lasted longer in the high-CHO group, amounting to 0.8 +/- 0.5, 3.4 +/- 0.6, and 9 +/- 1 g of lipid synthesized in the high-fat, mixed, and high-CHO groups, respectively. The thermic effect of the CHO load was 5.2 +/- 0.5% on the high-fat, 6.5 +/- 0.4% on the mixed diet, and 8.6 +/- 0.4% on the high-CHO diet. Significant relationships were demonstrated between the postabsorptive nonprotein respiratory quotient and net lipogenesis after the CHO load (r = 0.82) and between net lipogenesis and the increase in energy expenditure (r = 0.71). It is concluded that the antecedent diet influences the amount of net lipogenesis and the magnitude of thermogenesis after a large CHO test meal.
However, lipogenesis remains too limited even after such large CHO intakes to cause an increase in the body's fat content.
Hehe...
