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Abstract
The requisites for energy expenditure are covered mainly by two major substrates,
glucose and free fatty acids (FFA). Their regulation and metabolism differ. After
carbohydrate ingestion, glucose is rapidly oxidized or stored in muscles and liver.
There is a constant alternance between glucose storage as glycogen after meals and
glycogen mobilization in the postabsorptive state when plasma glucose has returned
to the basal state. Impairment of this alternance, in particular when glycogen stores
are not being used, may lead to glucose intolerance and insulin resistance. Ingestion
of lipids is not followed by an immediate increase in lipid oxidation, but FFA are
stored as triglycerides in different tissues. Lipolysis occurs in the fasting state
from tissue triglycerides and favors lipid oxidation. Lipid oxidation is typically
increased in obesity. The preferential use of FFA from triglyceride store for energy
expenditure in obesity is responsible for the decrease in glucose mobilization from
glycogen stores. This leads to a negative feedback of muscle and liver glycogen on
glycogen synthase activity and consequently on glucose storage. It results in glucose
intolerance after carbohydrate ingestion. Diabetes develops in obesity, usually after
a long period of glucose intolerance, when glycemia does not return to the basal state.
In obesity, glucose intolerance and insulin resistance can be prevented, or if already
existing, can be decreased by stimulating glycogen mobilization by exercise, thermogenesis-stimulating
drugs, and weight loss, which reduces fat stores and decreases lipid oxidation.
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© 1995 Published by Elsevier Inc.
