Adipose tissue glucose uptake

In adipose tissue glucose uptake is diminished and triglyceride breakdown is increased. The fatty acids produced are exported via the plasma and are oxidized by other tissues, while the glycerol is used for gluconeogenesis in the liver. Muscle oxidizes mainly fatty acids and ketone bodies while the brain adapts to use ketone bodies rather than glucose as a major energy source. This ability of the brain to use ketone bodies reduces the requirement for amino acids as a source of glucose, and is a factor of importance in the conservation of body protein. 

The rate of mitochondrial oxidations and ATP synthesis is continually adjusted to the needs of the cell (see reviews by Brand and Murphy 1987 Brown, 1992). Physical activity and the nutritional and endocrine states determine which substrates are oxidized by skeletal muscle. Insulin increases the utilization of glucose by promoting its uptake by muscle and by decreasing the availability of free long-chain fatty acids, and of acetoacetate and 3-hydroxybutyrate formed by fatty acid oxidation in the liver, secondary to decreased lipolysis in adipose tissue. Product inhibition of pyruvate dehydrogenase by NADH and acetyl-CoA formed by fatty acid oxidation decreases glucose oxidation in muscle. 

GLUT 4 Heart and skeletal muscle, adipose tissue Insulin-stimulated uptake of glucose... 

Answer C. Insulin increases glucose transport in only two tissues, adipose and muscle. The major site of glucose uptake is muscle, which decreases hyperglycemia. Glucose and ketone transport and metabolism are insulin independent in the brain (choice D). Insulin would slow gluconeogenesis (choice A) and fatty acid release from adipose (choice B). Insulin would inhibit glycogenolysis in the liver (choice E). 

GLUT 4 Skeletal muscle Adipose tissue 5 mM Insulin-stimulated glucose uptake... 

Figure 3.23 A sequence of processes explaining the role of glucokinase in the liver and fi-cells in regulation of the blood glucose concentration. The increase in the plasma insulin increases glucose uptake by muscle and decreases fatty acid mobilisation from adipose tissue which lowers the plasma fatty acid level which also increases glucose uptake (Chapter 12).

Changes in the blood levels of these hormones all contribute to regulation of blood glncose level in several conditions. After a meal glucose utilisation is increased, since insulin stimulates glucose uptake by muscle and inhibits release of fatty acids from adipose tissue. Physical activity... 

Blood-bome fuels are glucose, which is derived from liver glycogen, and fatty acids derived from adipose tissue. Uptake depends on the flow of blood through the muscle, the concentration of the fuel in the blood and the demand for ATP within the muscle. During sustained exercise the flow of blood to the muscle can increase up to 50-fold and the rate of utilisation of the fuel can increase to a similar extent, yet the concentration of the fuels in blood remains remarkably constant (Table 13.5). 

Figure 16.3 Effects of insulin on the glucose/fatty acid cycle. Insulin enhances glucose metabolism by stimulating glucose uptake by muscle and adipose tissue and by inhibiting lipolysis in adipose tissue (see Chapter 12 for the mechanism of these effects). The effect of glucose metabolism on lipolysis is via stimulation of fatty acid esterification via glycerol 3-phosphate.

Because digestion of food in the intestinal tract is dispensable and only counterproductive, the propulsion of intestinal contents is slowed to the extent that peristalsis diminishes and sphinc-teric tonus increases. However, in order to increase nutrient supply to heart and musculature, glucose from the liver and free fatty acid from adipose tissue must be released into the blood. The bronchi are dilated, enabling tidal volume and alveolar oxygen uptake to be increased. 

The biosynthesis and release of insulin by the pancreatic B cells (see p. 160) is stimulated by high blood glucose levels (> 5 mM). The insulin released then stimulates increased uptake and utilization of glucose by the cells of the muscle and adipose tissues. As a result, the blood glucose level falls back to its normal value, and further release of insulin stops. 

As it does in adipose tissue, insulin promotes increased glucose uptake by skeletal muscle. 

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