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Adipose Tissue Mass

FIGURE 14 Hypothetical regulatory system for maintaining constancy of adipose mass in which the mass of total stored fat is monitored. Adjustments in energy intake and expenditure are made to maintain constancy. Solid lines ( + ) denote increase; dashed arrows (—) denote decrease.

Adipose Tissue Mass

FIGURE 14 Hypothetical regulatory system for maintaining constancy of adipose mass in which the mass of total stored fat is monitored. Adjustments in energy intake and expenditure are made to maintain constancy. Solid lines ( + ) denote increase; dashed arrows (—) denote decrease.

with neurons in the arcuate and paraventricular nuclei that regulate secretion of hypophysiotropic hormones (see Chapter 38). Important advances have been made in our understanding of the complex process of regulating food intake in recent years including discovery of the adipocyte hormone, leptin, and some of the neuropep-tide transmitters associated with appetite control and their receptors.

response to nutritional status than to changes in adipose mass, it has been suggested that a fall in blood leptin concentration acts as a starvation signal to increase food intake and initiate energy conservation.

Leptin is encoded as a 167-amino-acid prohormone that is the product of the ob gene. Its tetrahelical structure resembles that of the class of cytokines and hormones that includes GH and prolactin. Because mRNA levels correlate with circulating leptin concentrations and with low levels of the hormone present in adipocytes, secretion of leptin is thought to be regulated at the level of gene transcription. Little is known of the cellular events that are associated with leptin secretion or of the mechanisms that regulate synthesis. Studies of isolated adipocytes indicate that enlargement of the lipid storage droplet increases leptin mRNA production, But the cellular mechanisms that are activated by fat cell enlargement are not understood. Insulin and cortisol act synergistically to increase leptin synthesis and secretion, whereas norepi-nephrine or increased activity of the sympathetic nervous system decreases leptin production. Plasma concentrations of leptin appear to follow a circadian pattern with highest levels found at night. Frequent spikes in leptin concentration in blood are indicative of synchronized pulsatile secretion, but how secretion by diffusely distributed adipocytes is coordinated is not understood. More than 40% of the leptin in blood is bound to protein. Leptin is cleared from the blood primarily by the kidney.

The leptin receptor, like receptors for GH and pro-lactin, belongs to the class of transmembrane cytokine

Leptin

Leptin, which means "thin," is expressed primarily, but not exclusively, in adipocytes. Inactivating mutations of the gene that encodes leptin or its receptor results in hyperphagia (excess food consumption), obesity, diabetes, impaired temperature regulation, and infertility in mice. In the very rare cases that have been reported in humans, mutation of the genes that code either for leptin or its receptor results in hyperphagia, morbid obesity, and impaired sexual development. When administered to obese, leptin-deficient mice, leptin decreases body weight by reducing food intake and increasing energy utilization (Fig. 15).

Leptin concentrations in blood correlate positively with body fat content (Fig. 16), suggesting that leptin might provide a means for monitoring fat stores. Blood levels of leptin also reflect changes in nutritional state. Within hours after initiation of fasting, leptin concentrations decrease sharply (Fig. 17) and, conversely, sustained overfeeding increases plasma levels. Because leptin concentrations change to a far greater extent in

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