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The Difference in the Storage Capacities for Carbohydrate and for Fat, and Its Implications in the Regulation of Body Weight a
Author(s) -
FLATT J. P.
Publication year - 1987
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1987.tb36202.x
Subject(s) - glycogen , palatability , carbohydrate , obesity , medicine , endocrinology , food science , biology , chemistry , zoology
The two-compartment model presented here suggests that weight maintenance can be achieved by a regulation of food intake geared primarily toward the maintenance of stable glycogen levels, rather than toward the preservation of the overall energy balance. This concept is reminiscent of the glucostatic theory of food intake regulation proposed by Mayer. It is viewed here as being linked to changes in the body's carbohydrate stores, which represent an integration of carbohydrate and lipid fluxes, rather than to changes in blood glucose levels, whose substantial variations during the day are dependent on various circumstantial events. The model illustrates that the fat to carbohydrate ratio of the diet may have considerable potential influence on steady state body composition, even though carbohydrates and fats are both able to meet the body's energy substrate requirements. It appears that failure of appropriately reducing the range within which glycogen levels are maintained when the diet's fat content rises will require an expansion of the adipose tissue mass to raise FFA levels and fat oxidation to a rate commensurate with the proportion of fat in the diet. Maintenance of glycogen reserves below their level of saturation is made less likely by the high palatability and ubiquitous availability of foods in affluent societies. Thus, one can understand the high incidence of obesity among populations consuming mixed diets with a relatively high fat content, without having to attribute this to some defect(s) in the mechanism(s) controlling food intake.