1. Chapter 8
Companion site for Basic Medical Endocrinology, 4th Edition Author: Dr. Goodman

2. Storage and utilization of biological fuels.
FIGURE 8.1
Storage and utilization of biological fuels.
Companion site for Basic Medical Endocrinology, 4th Edition. by Dr. Goodman
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FIGURE 8.2
Intraorgan flow of substrate and the competitive regulatory effects of glucose and fatty acids that comprise the glucose–fatty acid cycle. See text for details.
Companion site for Basic Medical Endocrinology, 4th Edition. by Dr. Goodman
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FIGURE 8.3
Actions of AMP activated protein kinase (AMPK) in muscle increase oxidation of fatty acids and glucose. Phosphorylation inactivates acetyl CoA carboxylase (ACC) and activates malonyl CoA decarboxylase (MCD). (See text for details.) TG = triglyceride; PL = phospholipids; DAG = diacylglycerol; FACoA = fatty acyl coenzyme A; ACT-1 = acyl carnitine transferase-1; FA-carnitine = fatty acyl carnitine.
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FIGURE 8.4
Multiple effects of AMP activated kinase (AMPK) that summate to increase energy producing reactions and inhibit energy consuming reactions.
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FIGURE 8.5
Interaction of hormones to maintain the blood glucose concentration. Green arrows denote increase; red arrows denote decrease.
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FIGURE 8.6
Counterregulatory hormonal responses to insulin-induced hypoglycemia. The infusion of insulin reduced plasma glucose concentration to 50 to 55 mg/dL. (From Sacca, L., Sherwin R., Hendler, R., and Felig P. (1979) Influence of continuous physiologic hyperinsulinemia on glucose kinetics and counterregulatory hormones in normal and diabetic humans. J. Clin. Invest. 63: 849–857.)
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FIGURE 8.7
Synergistic effects of cortisol, glucagon, and epinephrine on increasing plasma glucose concentration. Note that the hyperglycemic response to the triple hormone infusion is far greater than the additive response of all three hormones given singly. (Redrawn from data of Eigler, N., Sacca, L., and Sherwin, R.S. (1979) Synergistic interactions of physiologic increments of glucagon, epinephrine, and cortisol in the dog. J. Clin. Invest. 63: 114–123.)
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FIGURE 8.8
Hormonal effects on FFA production. Epinephrine and norepinephrine stimulate hormone-sensitive lipase through a cyclic AMP mediated process. Insulin antagonizes this effect by stimulating cyclic AMP degradation. T3, cortisol, and growth hormone increase the response of adipocytes to epinephrine and norepinephrine. Growth hormone also directly stimulates lipolysis. Insulin indirectly antagonizes the release of FFA by increasing reesterification. Growth hormone and cortisol increase FFA release by inhibiting reesterification.
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FIGURE 8.9
Effects of metabolic hormones on adipose tissue. *Lipolytic effects of cortisol are permissive.
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FIGURE 8.10
Effects of metabolic hormones on skeletal muscle. *The stimulation of fatty acid oxidation by growth hormone and cortisol are indirect and result from increased fatty acid mobilization.
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12. Effects of metabolic hormones on the liver.
FIGURE 8.11
Effects of metabolic hormones on the liver.
Companion site for Basic Medical Endocrinology, 4th Edition. by Dr. Goodman
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FIGURE 8.12
Quantitative turnover of substrates in a hypothetical person in the basal state after fasting for 24 hours [–1,800 calories]. (From Cahill, G.F. Jr. (1970) Starvation in man. N. Engl. J. Med. 282: 668–675.)
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FIGURE 8.13
Representative values for plasma glucose and metabolic hormones during fasting. Values for growth hormone are averaged over 24 hours. The small decline in cortisol may reflect a decrease in cortisol binding globulin.
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FIGURE 8.14
Effects of 1 day of fasting on GH secretion. A. Normal fed young man. B,L,D indicate meal times. GHRH (1μg/kg) was given intravenously at the time indicated by the arrow. B. GH concentrations in plasma in the same subject after a 24-hour fast. Blood was sampled every 20 minutes. Note that GH secretion is pulsatile and that the amplitudes of the spontaneous secretory bursts and the response to GHRH were increased by fasting. (From Ho, K.Y., Veldhuis, J.D., Johnson, M.L., Furlanetto, R., Evans, W.S., Alberti, K.G., Thorner, M.O. (1988) Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J. Clin. Invest. 81: 968.)
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FIGURE 8.15
Plasma concentrations of glucose in normal subjects and patients suffering from isolated deficiency of GH during control days of normal food intake and while fasting. Some GH-deficient patients were untreated and others were given 5 mg of hGH per day (treated). The fast began after the collection of blood on day 2. (From Merimee, T. J., Felig, P., Marliss, E., Fineberg, S.E., Cahill, G.F. Jr. (1971) Glucose and lipid homeostasis in the absence of human growth hormone. J. Clin. Invest. 50: 574–582.)
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FIGURE 8.16
Changes in sources of fuels utilized during prolonged exercise at 30% of maximal oxygen consumption. (Drawn from the data of Ahlborg, G., Felig, P., Hagenfeldt, L., Hendler, R., and Wahren, J. (1974) Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, free fatty acids, and amino acids J. Clin Invest. 53: 1080–1090.)
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FIGURE 8.17
Changes in concentration of insulin and counterregulatory hormones during prolonged moderate exercise. Values shown are the means obtained for eight young men exercising on a bicycle ergometer at ~50% of maximum oxygen consumption. (Drawn from data of Davis, S.N., Galassetti, P., Wasserman, D.H., and Tate, D. (2000) Effects of gender on neuroendocrine and metabolic counterregulatory responses to exercise in normal man. J. Clin. Endocrinol. Metab. 85: 224–230.)
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FIGURE 8.18
Postulated interaction between exercising muscle and resting muscle via the Cori cycle. (Redrawn from Ahlborg, G., Wahren, J., and Felig, P. (1986) Splanchnic and peripheral glucose and lactate metabolism during and after prolonged arm exercise. J. Clin. Invest. 77: 690–699.)
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FIGURE 8.19
Adipocyte differentiation. GH = growth hormone; IGF-I = insulin-like growth factor-I; TNF- = tumor necrosis factor-; PDGF = platelet-derived growth factor; FGF = fibroblast growth factor; EGF = epidermal growth factor; TGF-= transforming growth factor-; TGF-= transforming growth factor-.
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FIGURE 8.20
Data showing changes in body weight and fat content with aging obtained in five independent studies of individuals living in the early to middle decades of the twentieth century. (From Forbes, G.B., Reina, J.C. (1970) Adult lean body mass declines with age: Some longitudinal observations. Metabolism 19: 653–663.)
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FIGURE 8.21
Changes in energy expenditure after increase or decrease of body weight. Thirteen normal subjects were overfed a defined diet until their body weight increased by 10%. Eleven normal subjects were underfed until their body weight decreased by 10%. Both groups were then fed just enough to maintain their new weights for two weeks, at which time energy expenditure and lean body mass were measured. (Drawn from data of Leibel, R.L., Rosenbaum, M., Hirsch. (1995) Changes in energy expenditure resulting from altered body weight. N. Engl. J. Med. 332: 673–674.)
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FIGURE 8.22
Hypothetical regulatory system for maintaining constancy of adipose mass by monitoring the mass of stored fat. Adjustments in energy intake and expenditure are made to maintain constancy. Green arrows (+) denote increase; red arrows () denote decrease.
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FIGURE 8.23
Schematic drawing of the relationship between the principal neurons in the arcuate nuclei that control fuel consumption and energy utilization to each other and to their up- and downstream effectors. NPY = neuropeptide Y; NPYR = NPY receptor; AGRP = agouti related peptide; MCR4 = melanocortin receptor 4 (MSH receptor); MCH = melanin concentrating hormone; -MSH = - melanocyte stimulating hormone; CART = cocaine and amphetamine related transcript; GABA = gama amino butyric acid; GnRH = gonadotropin releasing hormone; CRH = corticotropin releasing hormone; TRH = thyrotropin releasing hormone; GHRH = growth hormone releasing hormone.
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FIGURE 8.24
Effects of leptin in leptin-deficient mice. Body weights of female obese mice treated with saline (Control) or 270 μg of leptin/day were compared to body weights of obese mice treated with saline, but were fed an amount of food equal to that consumed by the leptin-treated mice (pair-fed). Note that the loss of body weight produced by leptin was not accounted for simply by decreased food intake. (From Levin, N., Nelson, C., Gurney, A., Vandlen, R., de Sauvage, F. (1996) Pair-feeding studies provide compelling evidence that the ob protein exerts adipose-reducing effects in excess of those induced by reductions in food intake. Proc. Natl. Acad. Sci. USA 93: 1726–1730.)
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FIGURE 8.25
Leptin concentrations in blood plasma correlate with body fat content in 500 human subjects. (From Caro, J.F., Sinha, M.K., Kolaczynski, J.W., Zhang, P.L., Considine, R.V. (1996) Leptin: The tale of an obesity gene. Diabetes 45: 1455–1462.)
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FIGURE 8.26
Twenty-four-hour profiles of plasma concentrations of glucose and insulin in 15 obese and 14 age- and sex-matched normal subjects. The greater excursions of insulin values in the obese despite virtually identical levels of blood glucose are indicative of decreased sensitivity of liver, muscle, and adipose tissue to the actions of insulin. (From Polonsky, K., Given, B.D., and Van Cauter, E. (1988) Twenty-four-hour profiles and pulsatile patterns of insulin secretion in normal and obese subjects. J. Clin. Invest. 81: 442–448.)
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FIGURE 8.27
Overall regulation of energy balance. Ghrelin is the only known hunger signal arising from gut. All other input from the GI tract signal satiety. Leptin and insulin are the principal adiposity signals.
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FIGURE 8.28
Major routes of communication in the regulation of energy balance. Cross talk between the hypothalamus and the dorsal vagal complex integrates input from adiposity and satiety signals. The dorsal vagal complex includes the area postrema, the nucleus of the tractus solitarius, and the dorsal motor nucleus of the vagus. IL-6 = interleukin 6; CRH = corticotropin releasing hormone; MCH = melanin concentrating hormone; OXM = oxyntomodulin; PYY = peptide YY; CCK = cholecystokinin; GLP-1 = glucagon-like peptide-1; PPP = pancreatic polypeptide.
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