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Glucose hormones increasing

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. [Pg.209]

Factors that stimulate glucagon secretion include a decrease in blood glucose an increase in blood amino acids sympathetic nervous stimulation stress and exercise. Factors that inhibit glucagon secretion include insulin and an increase in blood glucose. Table 10.2 summarizes the major functions of the hormones discussed in this chapter. [Pg.138]

Metabolic Effects. Thyroid hormones affect energy substrate utilization in a number of ways. For instance, these hormones increase intestinal glucose absorption and increase the activity of several enzymes involved in carbohydrate metabolism. Thyroid hormones enhance lipolysis by increasing the response of fat cells to other lipolytic hormones. In general, these and other metabolic effects help to increase the availability of glucose and lipids for increased cellular activity. [Pg.461]

Figure 18.2. Endocrine-immune inter-relationship in normal subject. The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that includes the hypothalamus, the pituitary and the adrenal glands. The main hormones that activate the HPA axis are corticotrophin releasing factor (CRF), arginine vasopressin (AVP) and adrenocorticotrophic hormone (ACTH). The loop is completed by the negative feedback of cortisol on the hypothalamus and pituitary. The simultaneous release of cortisol into the circulation has a number of effects, including elevation of blood glucose for increased metabolic demand. Cortisol also negatively affects the immune system and prevents the release of immunotransmitters. Interference from other brain regions (e.g. hippocampus and amygdala) can also modify the HPA axis, as can neuropeptides and neurotransmitters. Figure 18.2. Endocrine-immune inter-relationship in normal subject. The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that includes the hypothalamus, the pituitary and the adrenal glands. The main hormones that activate the HPA axis are corticotrophin releasing factor (CRF), arginine vasopressin (AVP) and adrenocorticotrophic hormone (ACTH). The loop is completed by the negative feedback of cortisol on the hypothalamus and pituitary. The simultaneous release of cortisol into the circulation has a number of effects, including elevation of blood glucose for increased metabolic demand. Cortisol also negatively affects the immune system and prevents the release of immunotransmitters. Interference from other brain regions (e.g. hippocampus and amygdala) can also modify the HPA axis, as can neuropeptides and neurotransmitters.
The growth hormone response to intravenous glucose is increased in the postoperative period (R4). Although growth hormone is not necessary for the metabolic response to occur, it is suggested that the increased amounts in the circulation may be an attempt by the body to overcome some protein loss. However, data from patients undergoing hypophysec-tomy fail to show any alteration in the pattern of the catabolic response. [Pg.263]

Opposing the actions of insulin are the counterregulatory hormones, glucagon, epinephrine, growth hormone, and cortisol. In response to low blood glucose, the coxmterregu-latory hormones increase hepatic glucose... [Pg.2]

The answer is c. (Murray, pp 505—626. Scriver, pp 4029—4240. Sack, pp 121-138. Wilson, pp 287-320.) Vasopressin, which is also called antidiuretic hormone, increases the permeability of the collecting ducts and distal convoluted tubules of the kidney and thus allows passage of water. Like the mineralocorticoid aldosterone, vasopressin results in an expansion of blood volume. However, the mode of action of aldosterone is different it causes sodium reabsorption, not water reabsorption. Sodium reabsorption indirectly leads to increased plasma osmolality and thus water retention in the blood. Cortisol is a glucocorticoid that potentiates catabolic metabolism chronically. Epinephrine stimulates catabolic metabolism acutely. Insulin acutely favors anabolic metabolism, in large part by allowing glucose and amino acid transport into cells. [Pg.281]

Growth hormone increases the sensitivity of the adipocyte to the lipolytic action of the catecholamines and decreases its sensitivity to the lipogenic action of insulin. These actions lead to the release of free fatty acids and glycerol into the blood to be metabolized by the liver. GH also decreases esterification of fatty acids, thereby reducing triacylglycerol synthesis within the fat cell. Recent evidence suggests that GH may impair glucose uptake by both fat and muscle cells by a postreceptor inhibition of insulin action. [Pg.790]

In general, the thyroid hormone increases glucose level by glycogenolysis and gluconeogenesis, stimulates lipolysis especially in hyperthyroidism. In normal conditions, the thyroid hormone has stimulatory effects on the synthesis of proteins but also leads to catabolic reactions in muscle under hypo- and hyperthyroid states [10]. [Pg.232]

Peptides (short chains of amino acids, see Section 3.6.3), comprise the classes of hormones, neurotransmitters, endorphins, and growth factors. They are produced and stored in the nervous system, endocrine system, and immune system (Capra, 1996). They are physiologically active, and increase attention, raise glucose levels, increase heart rate, and deaden pain, among others. [Pg.449]

Control of secretion of anterior pituitary hormones also includes inhibition by hormones produced by target organs. For example, CRH stimulates the anterior pituitary to secrete ACTH, which in turn stimulates the adrenal cortex to secrete corticosteroids. Corticosteroids then feed back to inhibit the secretion of ACTH. Feedback mechanisms are important for the control of most hormones. For example, insulin (qv) secretion from the pancreas increases in response to increased blood glucose resulting from ingestion of a meal. Insulin increases tissue uptake and metaboHsm of glucose, which lowers blood glucose and in turn reduces insulin secretion. [Pg.171]

The primary hormone responsible for conversion of glucose to glycogen is insulin (Figure 6.36). Insulin is secreted by special cells in the pancreas called the islets of Langerhans. Secretion of insulin is a response to increased glucose in the... [Pg.758]


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