Skin medications an 627 buy cheap triamcinolone 4mg on line, plasma symptoms bone cancer best 4mg triamcinolone, and adrenal cortex contain 5575% of cholesterol in the esterified form symptoms pink eye buy 4 mg triamcinolone with mastercard. Storage lipid pool Triacylglycerols are the main energy storage form of lipids and they are the principal component of body fat treatment jones fracture buy 4mg triamcinolone with amex. The fatty acid profile of adult body fat always reflects the profile of dietary fat. Only rarely would this result in other fatty acids being more prevalent in body fat than the four listed here. At birth, the fatty acid profile of body fat is unusual in having very low linoleate (<3%) and -linolenate (<1%) but a higher proportion of longchain polyunsaturates than later in life. The main sites of body fat are subcutaneous and intravisceral, and they have different rates of response to stimuli for accumulation or release of fatty acids. The lipid composition and metabolic fate of these two pools are quite distinct, although many of the fatty acids occupying both pools are the same. The main components of both membrane and storage lipids are the long-chain (1624 carbons) saturated, monounsaturated, and polyunsaturated fatty acids. Although several of the major long-chain fatty acids in the body are common to both membrane and storage lipids, namely palmitate, stearate, oleate, and linoleate, three important distinctions exist between membrane and storage lipids. Structural lipid pool Biological membranes surrounding cells and subcellular organelles exist primarily as lipid bilayers (Figure 6. The lipids in both the inner and outer surfaces of membranes are composed mainly of phospholipids and free cholesterol, which interface with a myriad Nutrition and Metabolism of Lipids 105 Plasma and milk lipids In a way, plasma and milk lipids are an exception to the general rule distinguishing membrane and storage lipids. Free fatty acids are not components of lipoproteins but are transported bound to albumin. They are liberated mostly from adipose tissue when plasma glucose and insulin are low. Plasma also contains proportionally more fatty acids esterified to cholesterol (cholesteryl esters) than are found in tissues. Whole body content and organ profile of fatty acids An estimate of the whole body content of lipids in a healthy adult human is given in Table 6. Additional body fat is deposited during pregnancy, but the fatty acid composition remains similar to that of nonpregnant adults and reflects dietary fat intake. Docosahexaenoate also rises rapidly in brain lipids, followed a little later by an increasing content of long-chain saturates and monounsaturates as myelin develops. Adipose tissue contains very little linoleate or -linolenate at birth but their content increases rapidly with milk feeding. Plasma cholesterol is relatively low at birth and in infancy, but increases by more than twofold by adulthood. In general, regardless of the profile of dietary fatty acids, saturated and monounsaturated fatty acids predominate in adipose tissue, whereas there is a closer balance between saturates, monounsaturates, and polyunsaturates in structural lipids. It begins with acetyl-CoA being converted to malonyl-CoA by acetyl-CoA carboxylase, an enzyme dependent on biotin. This is subsequently reduced, dehydrated, and then hydrogenated to yield a four-carbon product that recycles through the same series of steps until the most common long-chain fatty acid product, palmitate, is produced (Figure 6. Thus, the transfer of acetyl-CoA to the cytosol for fatty acid synthesis appears to require its conversion to citrate to exit the mitochondria before being reconverted to acetyl-CoA in the cytosol. There are three main features of long-chain fatty acid synthesis in mammals: 1 inhibition by starvation 2 stimulation by feeding carbohydrate after fasting 3 general inhibition by dietary fat. Carbohydrate is an important source of carbon for generating acetyl-CoA and citrate used in fatty acid synthesis. Acetyl-CoA carboxylase is a key control point in the pathway and is both activated and induced to polymerize by citrate. The individual steps occur with the substrate being anchored to the acyl carrier protein. This is probably one important negative feedback mechanism by which both starvation and dietary fat decrease fatty acid synthesis. High amounts of free long-chain fatty acids would also compete for CoA, leading to their -oxidation. Humans consuming >25% dietary fat synthesize relatively low amounts of fat (<2 g/day). Compared with other animals, humans also appear to have a relatively low capacity to convert stearate to oleate and linoleate or -linolenate to the respective longer chain polyunsaturates. Nevertheless, fatty acid synthesis is stimulated by fasting/ refeeding or weight cycling, so these perturbations in Figure 6. The steps shown follow fatty acid "activation" (binding to coenzyme A) and carnitine-dependent transport to the inner surface of the mitochondria. Unsaturated fatty acids require additional steps to remove the double bonds before continuing with the pathway shown. They are then translocated inside the mitochondria by carnitine acyl-transferases. The -oxidation process involves repeated dehydrogenation at sequential two-carbon steps and reduction of the associated flavoproteins (Figure 6. Nutrition and Metabolism of Lipids 107 the efficiency of fatty acid oxidation depends on the availability of oxaloacetate and, hence, concurrent carbohydrate oxidation. In contrast, -oxidation of unsaturated fatty acids yields a double bond in a different position that then requires further isomerization or hydrogenation. From a biochemical perspective, this extra step appears to make the oxidation of unsaturated fatty acids less efficient than that of saturated fatty acids. However, abundant in vivo and in vitro research in both humans and animals clearly shows that long-chain cis-unsaturated fatty acids with one to three double bonds (oleate, linoleate, -linolenate) are more readily -oxidized than saturated fatty acids of equivalent chain length, such as palmitate and stearate. This peroxisomal detour has been identified as an obligatory step in the endogenous synthesis of docosahexaenoate from eicosapentaenoate. Odd-carbon long-chain fatty acids are relatively uncommon but, when -oxidized, yield propionylCoA, the further -oxidation of which requires biotin and vitamin B12 as coenzymes. Ketogenesis and ketosis Large amounts of free fatty acids inhibit glycolysis and the enzymes of the tricarboxylic acid cycle, thereby impairing production of oxaloacetate. When insufficient oxaloacetate is available to support the continued oxidation of acetyl-CoA, two acetyl-CoA molecules condense to form a ketone, acetoacetate. Acetoacetate can be spontaneously decarboxylated to form acetone, a volatile ketone, or converted to a third ketone, -hydroxybutyrate. When glucose is limiting, ketones are an alternative source of energy for certain organs, particularly the brain. They are also efficient substrates for lipid synthesis during early postnatal development. Conditions favoring ketogenesis include starvation, diabetes, and a very high-fat, lowcarbohydrate "ketogenic" diet. Carbon recycling Carbon recycling is the process by which acetyl-CoA derived from -oxidation of one fatty acid is incorporated into another lipid instead of completing the -oxidation process to carbon dioxide. Carbon recycling of linoleate in the rat captures similar amounts of the linoleate skeleton to those of arachidonate, the main desaturation and chain-elongation product of linoleate. Peroxidation Peroxidation (auto-oxidation) is the nonenzyme-catalyzed reaction of molecular oxygen with organic compounds to form peroxides and related breakdown products. Initiating agents such as pre-existing peroxides, transition metals, or ultraviolet or ionizing radiation produce singlet oxygen. Singlet oxygen can then abstract hydrogen at the double bonds of polyunsaturates to produce free (peroxy) radicals, which abstract further hydrogens from the same or different fatty acids and propagate the peroxidation process. Eventually, this leads to termination by the formation of stable degradation products or hydroperoxides (Figure 6. Hydroperoxides can form further hydroperoxy radicals or can be reduced by antioxidants, which contain thiol groups, i. Since peroxidation is a feature of polyunsaturates, it is a potential hazard facing most membranes and dietary lipids. Humans and animals readily detect peroxidized fats in foods by their disagreeable odor and avoid them. However, modeling the effects of peroxides produced in vivo and in vitro is particularly challenging because lipid peroxidation undoubtedly is an important part of several necessary biological processes such as activation of the immune response. Desaturation, chain elongation, and chain shortening One important characteristic of long-chain fatty acid metabolism in both plants and animals is the capacity to convert one to another via the processes of desaturation, chain elongation, and chain shortening.
Human protein requirements: assessment of the adequacy of the current Recommended Dietary Allowance for dietary protein in elderly men and women symptoms zinc toxicity discount 4mg triamcinolone mastercard. A physiologic bases for the provision of fuel mixtures in normal and stressed patients 97110 treatment code effective triamcinolone 4 mg. The possibility of acute inflammatory reaction affects the development of pressure ulcers in bedridden elderly patients symptoms 8 weeks pregnant generic 4mg triamcinolone. Implication of cytokines in the aggravation of malnutrition and hypercatabolism in elderly patients with severe pressure sores treatment xdr tb guidelines triamcinolone 4 mg low cost. Association between the soluble interleukin-2 receptor and serum markers of malnutrition. Plasma cytokine levels in cardiac chambers of patients with mitral stensis with congestive heart failure. Enhanced generation of interleukin 1 and 6 may contribute to the cachexia of chronic disease. Hypothalamic concentration and release of neuropeptide Y into microdialyses is reduced in anorectic tumor bearing rats. Neurochemical-neuroendocrine systems in the brain controlling macronutrient intake and metabolism. Low circulation leptin level in protein-energy malnourished chronically ill elderly patients. A prospective, randomized, double-blind, controlled clinical trial of enteral immunonutrition in the critically ill. A controlled trial of megestrol acetate on appetite, caloric intake, nutritional status, and other symptoms in patients with advance cancer. Megestrol acetate therapy for anorexia and weight loss in children with malignant solid tumours. Megestrol Acetate in Neoplastic Anorexia/Cachexia: Clinical Evaluation and Comparison with Cytokine Levels in Patients with Head and Neck Carcinoma Treated with Neoadjuvant Chemotherapy. The delayed hypersensitivity response and host resistance in surgical patients: 20 years later. Air-fluidized beds or conventional therapy for pressure sores: a randomized trial. Clinical utility and cost-effectiveness of an air suspension bed in the prevention of pressure ulcers. Risk factors for pressure sores: a comparison of cross-sectional and cohort-derived data. Occurrence and predictors of pressure sores in the National Health and Nutrition Examination Survey follow-up. The incidence of vertebral and hip fractures increases exponentially with advancing age (while that of wrist fractures plateaus after the age of 60 511 512 Geriatric Nutrition years). The paradox that hip fracture rates are higher in developed countries, where calcium intake is higher than in developing countries, clearly calls for an explanation. The report also acknowledged that strong evidence was emerging that the requirements for calcium might vary from culture to culture for dietary, genetic, lifestyle, and geographical reasons. Within these limitations, this chapter will attempt to review the available data for micronutrients as they apply to fracture prevention in the elderly. Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to bone fragility and a consequent increased risk of fracture. Collagen type I is the most abundant organic molecule, while crystals containing calcium and phosphorus make up most of the inorganic weight. Highly regulated at local, distant, and central levels, cells of the skeleton, the osteoclasts, which resorb bone, and the osteoblasts, which lay down new bone, are part of a process to afford the individual with adequate support for locomotion and a ready store of essential ions for homeostasis. Variations in tissue mineral density affect function, such as the enamel of teeth having the highest tissue density of calcium. The enzymes responsible for this cross-linking require trace metals for normal functioning. In osteoporosis and aging, there are reports of increased magnesium content and decreased fluoride, acid phosphate, boron, strontium, and carbonate contents. Variation in mineral content in osteoporosis is important, but other material properties beyond content alone contribute to the loss of mechanical strength in osteoporotic bones. Note that the plant source of vitamin D is called ergocalciferol (D2) and animal vitamin D is called cholecalciferol (D3). For reasons of clarity, vitamin D will refer to all forms of vitamin D unless otherwise stated. First, an organic matrix is laid down, or osteoid; only then can subsequent mineralization occur. During the lifetime of an individual, bone responds to increased loads by increasing bone matrix and bone mineralization as well as repairing microcracks that result from fatigue damage. Similarly, loss of bone may also occur at different rates, depending on the bone and age of the individual. This discussion of micronutrients must therefore consider effects on bone formation, bone resorption, or both, when addressing mechanisms of dietary interventions. Particular problems with regard to bone density interpretation that are specific to the elderly population are the development of osteoarthritis and vascular calcification. One must also consider in the evaluation of fracture studies effects on falls that are independent of changes in bone mineral density. The absorption, distribution, and excretion of micronutrients may also be altered in the geriatric patient, and this population must be evaluated before making recommendations. The issue of interaction with another micronutrient must also be considered when evaluating interventions with such minute quantities. Based on the bone mineral density exam, one cannot readily distinguish between osteomalacia, a condition of undermineralized bone, and osteoporosis, as Fuller Allbright put it, the lack of bone in bone. One should note, however, that bone histomorphometry shows the absence of bone, not the absence of crystallization. Decreased calcium intake, impaired intestinal absorption of calcium due to aging or disease, as well as vitamin D deficiency can result in secondary hyperparathyroidism. A sophisticated system of absorption, storage, release during lactation, and excretion in a manner that maintains the delicate balance between mineralization and dissolution has evolved to maintain optimal extracellular calcium concentration. Sustaining this depot requires adequate calcium absorption to overcome the obligatory losses of calcium through urine, feces, and sweat. This system must also regulate the highest rates of calcium accrual at a mean age of 121/2 years in girls and 14 years in boys. During the perimenopausal period, bone resorption accelerates, causing substantial losses of bone. Efforts by some investigators to correlate changes in bone mineral density to dietary intake of calcium in otherwise normal postmenopausal women have not always been successful. This study was placebo controlled and double blinded Nutrition and Fracture Risk 517 for the placebo and calcium arms. The classical way for this to be determined was by the use of calcium balance studies. In a review of 212 balances,34 the calcium requirement was calculated to be 500 to 600 mg daily. If elderly individuals are losing bone, then calcium supplementation must overcome this deficit to maintain adequate calcium stores. This transport may occur through a vitamin D-dependent saturable transcellular means or a nonsaturable paracellular pathway. At the duodenum, gastric acidity is still effective in generating ionized calcium, whereas biliary and pancreatic juices neutralize the acid in the more distal portions of the intestine. Renal Ca2+ absorption occurs in the proximal tubules where 70% of the filtered load is reabsorbed. Twenty percenet of filtered calcium is absorbed at the loop of Henle, and this process requires the protein paracellin-1. Reported median calcium intake was 433 mg/day for calcium supplement nonusers and 1319 (8451874) mg for calcium supplement users. It is also important to recognize that mineralization of bone occurs after the matrix is produced and not before.
The major physiologic role of flutathione peroxidase is to maintain appropriately low levels of hydrogen peroxides within cells symptoms before period purchase triamcinolone 4 mg online, thus decreasing potential free radical damage medicine knowledge order 4mg triamcinolone fast delivery. Selenium deficiency is accompanied by a decrease in glutathione peroxidase activity and results in an increase in hepatic glutathione-Stransferase activity medicine rash discount 4 mg triamcinolone with mastercard. Glutathione-S-transferase catalyzes the conjugation of electrophilic compounds and metabolites with glutathione medicine cabinets with lights order triamcinolone 4 mg line, which is an important hepatic detoxification mechanism. Selenium deficiency also increases liver glutathione synthesis, which can lead to a depletion of cysteine and impairment of protein synthesis. Selenium has also been demonstrated to alter other drug (xenobiotic)-metabolizing enzymes in addition to gluthathione-S-transferase. Thus, selenium deficiency clearly affects the ability of an individual to metabolize drugs. The selenium content of food is directly dependent on the soil concentration of selenium. Selenium intakes vary widely throughout the world, with intakes between 7 and 38,000 µg/day having been reported. An adequate selenium intake has been estimated at 50 µg/day, with toxic levels estimated to occur with intakes of the order of 350 to 700 µg/day. It appears that selenium in the form of selenomethionine (the form found in wheat) results in better selenium retention than does selenate or selenite. Circulating selenium concentrations either fall slightly79 or remain stable with aging. Selenium deficiency may be associated with a number of pathologic conditions (Table 11. The disease state best shown to be produced by selenium deficiency is a cardiomyopathy of children and young women (Keshan disease). Although selenium deficiency provides the necessary setting for the development of cardiomyopathy, other factors, such as viral infections, seem to play a role in the pathogenesis of this disease. One of the highest concentrations of selenium in the body is in the thyroid gland. Selenium plays a role through glutathione peroxidase in iodination of thyroglobulin. The enzyme responsible for conversion of thyroxine to triodothyronine is selenium dependent. There is a lower prevalence of cancer in countries with a high selenium concentration in the soil, such as Venezuela. Many case-controlled prospective studies have suggested a relationship of selenium deficiency to cancer risk. Reductions in cancer were most prominent in smokers and those who had the lowest selenium levels. Two controlled trials in China also suggested that selenium supplementation reduced cancer occurrence. This observation was supported by the finding that serum selenium levels correlated with the eicospentanoic acid concentrations. Studies in children have suggested that selenium-deficient kwashiorkor patients may fail to thrive until they receive selenium supplementation. An early sign of selenium overexposure is the development of a garlic odor on the breath. Other toxic effects include gastrointestinal disturbances, dizziness, and sweating. Selenium supplementation or choosing a selenium-supplemented formula should be considered in elderly subjects who are tube fed. Silicon deficiency may play a role in the development of such degenerative 188 Geriatric Nutrition diseases as osteoarthritis or atherosclerosis. The silicon content of certain animal tissues, such as the aorta, skin, and thymus, decreases with aging, whereas the content is unchanged in most tissues. Tin stimulates the production of hemoxygenase, which results in the elaboration of endogenous carbon monoxide. Recently, carbon monoxide has been suggested to play a role as a neurotransmitter and may play a role in appetite regulation. Studies on alterations in the intake or excretion of vanadium in older individuals have not been undertaken. It plays a key role in four areas: cell proliferation and growth, apoptosis, immune function, and oxidative metabolism. Zinc has been shown to play a role in modulating some of the polymorphisms associated with longevity. Measurement of zinc status is difficult with multiple factors from infection to exercise altering serum zinc levels. Dietary studies in older persons suggest that on the average they ingest less than the estimated average requirement of 9. Diuretics, diabetes mellitus, lung cancer, and cirrhosis of the liver are associated with hyperzincuria. Three double-blind studies support the concept that zinc replacement improves cellular immunity in zinc-deficient older persons. Excess zinc (40 mg/day) leads to impaired immune responses, abnormal copper metabolism, and adverse cholesterol patterns. There is a clear need for adequately powered 190 Geriatric Nutrition trials of zinc replacement in older persons with zinc deficiency to demonstrate its utility in improving the quality of life of older persons. Thus, high intakes of zinc, cadmium, or copper interfere with the utilization and tissue storage of iron. Enzymes involved in collagen cross-linking, one of the benchmarks of aging, are often catalyzed by trace elements. Selenium deficiency may play a role in carcinogenesis, is associated with immune dysfunction, and occurs commonly in tube-fed patients. Selenium is essential for the activity of glutathionine peroxidase, which protects against free radical damage by decreasing the formation of hydroxy radicals. Zinc appears to play an important role in immunity, macular degeneration, anorexia, taste abnormalities, and wound healing. Little is known about the role of drugs, especially diuretics, and intercurrent illness on the development of trace mineral deficiency with advancing age. Also, the interactions of trace elements with one another-particularly in the situation where the decision is made to replace a single trace element-need further investigation. Overall, there is a need for increased study of the role of trace elements in the aging process. World Health Organization, Evaluation of Certain Food Additives and the Contaminants Mercury, Lead and Cadmium, Technical Report Series 505, Geneva, 1972. A single nutrient (zinc) and some target genes related to inflammatory/immune response, Mech. Lennard-Jones, 1992 the nutritional status of older adults living at home is poor. Energy intakes of older men (40 to 74 years old) range from 2100 to 2300 calories/day compared to younger men (24 to 34 years old), who consume 2700 calories/day. Acute illness is characterized by a spontaneous decrease in food intake,9 a paradoxical response in the face of a need for increased nutrients during healing. A reduction in food intake accompanying acute illness occurs both before and during hospitalization. In the month before hospitalization, 65% of the males and 69% of the females had an insufficient energy intake, and undernutrition was present in 53% of males and 61% of females by the time of admission to the hospital. In 286 general medical subjects, 27% became malnourished during hospital admission. These subjects were more likely to consume less than 40% of prescribed food and were more likely to have lower Mini-Mental Status Examination scores, functional impairment, lower total lymphocyte counts, and lower serum albumin levels. When patients who had no current nutritional deficits and no predicted risk of developing deficits at hospital admission were followed, significant decreases in albumin, total lymphocyte count, triceps skinfold thickness, and midarm circumference occurred in all patients by 3 weeks. The only nutritional parameter remaining unchanged at 3 weeks was percent of ideal body weight. Persons who are identified as undernourished have higher mortality, a higher rate of life-threatening complications, longer hospital stays, higher comorbidities, more infections, and oxidative stress leading potentially to degenerative disease than persons who are considered well nourished2628 (see Table 12. Weight loss of more than 5% in women 60 to 74 years old has been associated with a two-fold increase in risk of disability over time, compared to women who did not lose weight.
Syndromes
Ages 69 and older: 17 - 90 ug/dL
Tuberculosis
Surgery for cancer
Blood clots in the legs that may travel to the lungs
Corticosteroid creams to treat skin rashes
Drink about 16 ounces (2 cups) of water 2 hours before a workout. It is important to start exercising with enough water in your body.
Glycogen medicine used during the civil war cheap 4mg triamcinolone amex, the storage form of glucose medicine qd purchase triamcinolone 4 mg without prescription, is present in most body tissues medicine 5277 buy discount triamcinolone 4mg line, but the major supplies are in the liver and skeletal muscle medicine 7 year program buy triamcinolone 4mg cheap. Glucose catabolism proceeds via cleavage through fructose to trioses or via oxidation and decarboxylation to pentoses. The pathway to pyruvate through the trioses is the EmbdenMeyerhof pathway, and that through 6-phosphogluconate and the pentoses is the direct oxidative pathway (hexose monophosphate shunt). Interconversions between carbohydrate, fat, and protein include conversion of the glycerol from fats to dihydroxyacetone phosphate and conversion of a number of amino acids with carbon skeletons resembling intermediates in the EmbdenMeyerhof pathway and citric acid cycle to these intermediates by deamination. In this way, and by conversion of lactate to glucose, nonglucose molecules can be converted to glucose (gluconeogenesis). Glucose can be converted to fats through acetyl-CoA, but because the conversion of pyruvate to acetyl-CoA, unlike most reactions in glycolysis, is irreversible, fats are not converted to glucose via this pathway. The major entry into it is through acetylCoA, but a number of amino acids can be converted to citric acid cycle intermediates by deamination. The citric acid cycle requires O2 and does not function under anaerobic conditions. All these reactions occur in the absence of O2 and consequently represent anaerobic production of energy. The numbers (6C, 5C, etc) indicate the number of carbon atoms in each of the intermediates. The pentoses formed in the process are building blocks for nucleotides (see below). To bring about any net change in a particular metabolic process, regulatory factors obviously must drive a chemical reaction in one direction. Most of the reactions in intermediary metabolism are freely reversible, but there are a number of "directional-flow valves," ie, reactions that proceed in one direction under the influence of one enzyme or transport mechanism and in the opposite direction under the influence of another. Five examples in the intermediary metabolism of carbohydrate are shown in Figure 123. The different pathways for fatty acid synthesis and catabolism (see below) are another example. Regulatory factors exert their influence on metabolism by acting directly or indirectly at these directional-flow valves. The breakdown of glycogen in 1:4 linkage is catalyzed by phosphorylase, whereas another enzyme catalyzes the breakdown of glycogen in 1:6 linkage. The principal determinants are therefore the dietary intake; the rate of entry into the cells of muscle, adipose tissue, and other organs; and the glucostatic activity of the liver (Figure 125). Five percent of ingested glucose is promptly converted into glycogen in the liver, and 3040% is converted into fat. During fasting, liver glycogen is broken down and the liver adds glucose to the bloodstream. With more prolonged fasting, glycogen is depleted and there is increased gluconeogenesis from amino acids and glycerol in the liver. Plasma glucose declines modestly to about 60 mg/dL during prolonged starvation in normal individuals, but symptoms of hypoglycemia do not occur because gluconeogenesis prevents any further fall. In carbohydrate metabolism there are several reactions that proceed in one direction by one mechanism and in the other direction by a different mechanism, termed "directional-flow valves. Pyruvate is converted to malate in mitochondria, and the malate diffuses out of the mitochondria to the cytosol, where it is converted to phosphoenolpyruvate. It is cycled: built up from glucose 6-phosphate when energy is stored and broken down to glucose 6-phosphate when energy is required. Note the intermediate glucose 1-phosphate and enzymatic control by phosphorylase a and glycogen kinase. Fructose 6-phosphate can also be phosphorylated in the 2 position, forming fructose 2,6-diphosphate. When the fructose 2,6-diphosphate level is high, conversion of fructose 6-phosphate to fructose 1,6-diphosphate is facilitated, and thus breakdown of glucose to pyruvate is increased. A decreased level of fructose 2,6-diphosphate facilitates the reverse reaction and consequently aids gluconeogenesis. Notice the glucostatic function of the liver, as well as the loss of glucose in the urine when the renal threshold is exceeded (dashed arrows). They may be saturated (no double bonds) or unsaturated (dehydrogenated, with various numbers of double bonds). The phospholipids are constituents of cell membranes and provide structural components of the cell membrane, as well as an important source of intra- and intercellular signaling molecules. Fructose is converted in part to fructose 6-phosphate and then metabolized via fructose 1,6-diphosphate. The enzyme catalyzing the formation of fructose 6-phosphate is hexokinase, the same enzyme that catalyzes the conversion of glucose to glucose 6-phosphate. However, much more fructose is converted to fructose 1-phosphate in a reaction catalyzed by fructokinase. Most of the fructose 1-phosphate is then split into dihydroxyacetone phosphate and glyceraldehyde. The glyceraldehyde is phosphorylated, and it and the dihydroxyacetone phosphate enter the pathways for glucose metabolism. Because the reactions proceeding through phosphorylation of fructose in the 1 position can occur at a normal rate in the absence of insulin, it has been recommended that fructose be given to diabetics to replenish their carbohydrate stores. Fatty acid oxidation begins with activation (formation of the CoA derivative) of the fatty acid, a reaction that occurs both inside and outside the mitochondria. Medium- and short-chain fatty acids can enter the mitochondria without difficulty, but long-chain fatty acids must be bound to carnitine in ester linkage before they can cross the inner mitochondrial membrane. Carnitine is -hydroxy-trimethylammonium butyrate, and it is synthesized in the body from lysine and methionine. In the liver, which (unlike other tissues) contains a deacylase, free acetoacetate is formed. The fat depots obviously vary in size, but in nonobese individuals they make up about 15% of body weight in men and 21% in women. They are not the inert structures they were once thought to be but, rather, active dynamic tissues undergoing continuous breakdown and resynthesis. In the depots, glucose is metabolized to fatty acids, and neutral fats are synthesized. Neutral fat is also broken down, and free fatty acids are released into the circulation. A third, special type of lipid is brown fat, which makes up a small percentage of total body fat. Brown fat, which is somewhat more abundant in infants but is present in adults as well, is located between the scapulas, at the nape of the neck, along the great vessels in the thorax and abdomen, and in other scattered locations in the body. In brown fat depots, the fat cells as well as the blood vessels have an extensive sympathetic innervation. This is in contrast to white fat depots, in which some fat cells may be innervated but the principal sympathetic innervation is solely on blood vessels. In addition, ordinary lipocytes have only a single large droplet of white fat, whereas brown fat cells contain several small droplets of fat. Sphingomyelins: Esters of fatty acid, phosphate, choline, and the amino alcohol sphingosine. Sterols: Cholesterol and its derivatives, including steroid hormones, bile acids, and various vitamins. The six families of lipoproteins (Table 15) are graded in size and lipid content. The density of these lipoproteins is inversely proportionate to their lipid content. In general, the lipoproteins consist of a hydrophobic core of triglycerides and cholesteryl esters surrounded by phospholipids and protein. These lipoproteins can be transported from the intestine to the liver via an exogenous pathway, and between other tissues via an endogenous pathway. These micelles additionally can contain important water-insoluble molecules such as vitamins A, D, E, and K. These mixed micelles are taken up into cells of the intestinal the liver, they diffuse into the circulation. Acetoacetate is also formed in the liver via the formation of 3-hydroxy-3-methylglutaryl-CoA, and this pathway is quantitatively more important than deacylation. An imbalance of ketone bodies can lead to serious health problems (Clinical Box 13). This process, splitting off two carbon fragments at a time, is repeated to the end of the chain.
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