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1. |
Guest Editorial: Recent Advances in Clinical Nutrition: The Role of the NIH-Supported General Clinical Research Centers |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 1-2
RudmanDaniel,
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ISSN:0731-5724
DOI:10.1080/07315724.1989.10737964
出版商:Routledge
年代:1989
数据来源: Taylor
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2. |
Advances in Hospital Nutrition |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 3-12
BistrianBruce R.,
JaksicThomas,
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ISSN:0731-5724
DOI:10.1080/07315724.1989.10737965
出版商:Routledge
年代:1989
数据来源: Taylor
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3. |
Obesity |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 13-21
DietzWilliam H.,
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摘要:
Over the past 20 years, obesity has represented a significant focus of research conducted in Clinical Research Centers (CRCs) in the United States. This review will focus on the progress in our understanding of the disease that CRC-based research has produced; therefore, the reference list is not exhaustive and consists primarily of CRC-based research. Obesity is defined as an excess of body fat as measured by triceps skinfold thickness. The time of onset of obesity is an important factor, for example, early onset is associated with an increase in the number of fat cells. Weight loss reduces the size but not the number of fat cells. Type II diabetes mellitus is a common complication in obese adults; this condition has been related to fat cell size and, in women, to predominantly upper-body fat distribution. Pregnant obese women and their babies are at risk for a number of problems. Abnormalities commonly found in obese persons include increased plasma lipid levels, hyperinsulinism, increased cholesterol synthesis, high frequency of gallstones, and hypertension. Under a variety of experimental conditions, the only difference in the response of obese and normal weight subjects to food was that the obese subjects appeared to consume more, but other data suggest that the obese may have greater energy needs. Carbohydrate intake has been studied extensively. Metabolic rate increases with overfeeding, especially in response to carbohydrate. Basal metabolic rates are higher in obese adults and rise in response to overfeeding; they decrease after weight reduction. This decrease can be counteracted with sucrose, perhaps because sucrose maintains triiodothyronine levels. Obese persons may be less able to dispose of excess calories. Carbohydrate-free diets have received intensive investigation, and the importance of high quality protein intakes and adequate mineral supplementation have been documented. Nonetheless, because of the limited success of hypocaloric diets for the severely obese, various surgical approaches have been explored.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737966
出版商:Routledge
年代:1989
数据来源: Taylor
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4. |
Advances in Infant Nutrition over the Past Quarter Century |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 22-32
HeirdWilliam C.,
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ISSN:0731-5724
DOI:10.1080/07315724.1989.10737967
出版商:Routledge
年代:1989
数据来源: Taylor
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5. |
Nutritional Management of Plasma Lipid Disorders |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 33-45
MargolisSimeon,
DobsAdrian S.,
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摘要:
Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2subtraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides;ω-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLchlevels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737968
出版商:Routledge
年代:1989
数据来源: Taylor
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6. |
Calcium Metabolism |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 46-53
PakCharles Y. C.,
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摘要:
In normal individuals, 1,25-dihydroxyvitamin D (1,25-D) levels regulate calcium (Ca) absorption according to Ca intake; its synthesis is stimulated by low Ca intake, probably via increased parathyroid hormone (PTH) secretion, to increase Ca absorption, and suppressed during high intake to reduce Ca absorption. The body also adapts Ca absorption in response to renal Ca excretion, and phosphate absorption in response to phosphate intake. These adaptations may fail or be impaired in certain diseases. In disorders of overadaptation, the intestinal tract absorbs excessive amounts of Ca due to overproduction of 1,25-D, as in absorptive hypercalciuria, sarcoidosis, primary hyperparathyroidism, and tumoral calcinosis. Intestinal hyperabsorption and hypercalciuria may occur on both low-and high-Ca diets. Primary hyperparathyroidism and hypoparathyroidism are bihormonal, related to over-and underproduction, respectively, of both 1,25-D and PTH. Underadaptation disorders are typically related to low 1,25-D synthesis or resistance to this metabolite; examples include postmenopausal osteoporosis, chronic renal failure, and osteomalacia. Many of these adaptational disorders can be relieved or improved by manipulating Ca, phosphate, sodium, or protein intake or by administering exogenous 1,25-D. Overabsorption of Ca and other substances, such as oxalate, may be responsible for Ca nephrolithiasis. Hypocitraturia (which may be a complication of certain diseases or the result of unbalanced diet or excessive exercise), diets high in readily metabolizable sugars and purine-rich proteins (meat, poultry, and fish), and low fluid intake can all contribute to stone formation. Various regimens may reduce the risk of Ca nephrolithiasis.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737969
出版商:Routledge
年代:1989
数据来源: Taylor
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7. |
Nutritional Therapy for Selected Inborn Errors of Metabolism |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 54-60
LevyHarvey L.,
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摘要:
Nutritional approaches are available for the management of several different classes of inborn metabolism errors. In phenylketonuria (PKU), phenylalanine is not properly metabolized; and its accumulation leads to neurologic dysfunction and metal retardation. Altering the diet to limit phenylalanine intake led to remarkable improvement in children with PKU. It was later found that instituting dietary therapy immediately after identification of the disorder in newborns prevented mental retardation. Throughout the 1960s nutritional therapies were found for other inborn disorders, including galactosemia, maple syrup urine disease, and homocystinuria. For the group of disorders associated with defects in the urea cycle, leading to profound hyperammonemia, therapy based on the concept of waste nitrogen excretion (i.e., by increasing excretion of urea cycle intermediates in the urine, nitrogen that would otherwise recycle as ammonia can be eliminated) dramatically produced better control of hyperammonemia and its consequences. Some inbom errors of metabolism respond to vitamin therapy. Biotin-related multiple carboxylase synthetase deficiency can be produced by either of two enzyme defects—holocarboxylase synthetase deficiency or biotinidase deficiency. Both are treatable with biotin supplementation. The symptoms of multiple carboxylase deficiency can also occur after intestinal resection or ingestion of raw eggs. Multiple carboxylase deficiency has been treated successfully in utero by giving the mother biotin supplements. Peroxisomal disorders may respond to dietary management. Liver disease in hereditary tyrosinemia may be accentuated by hypermethioninemia and treated by controlling the blood methionine level. Glycogen storage disease Type I, which causes hypoglycemia, can be controlled by oral administration of cornstarch.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737970
出版商:Routledge
年代:1989
数据来源: Taylor
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8. |
Recent Advances in Carbohydrate Nutrition and Metabolism in Diabetes Mellitus |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 61-67
AndersonJames W.,
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摘要:
The last decade has brought a tremendous turnaround in nutritional recommendations for diabetes management, moving from low-carbohydrate, high-fat diets to high-carbohydrate, high-fiber, low-fat diets. Clinical studies which furthered understanding of carbohydrate metabolism greatly contributed to the change. This paper reviews recent advances in selected aspects of carbohydrate nutrition and metabolism in diabetes mellitus.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737971
出版商:Routledge
年代:1989
数据来源: Taylor
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9. |
The Role of Dietary Electrolytes in Hypertension |
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Journal of the American College of Nutrition,
Volume 8,
Issue sup1,
1989,
Page 68-80
MooreThomas J.,
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摘要:
The possible contribution of dietary electrolyte intake as a cause of or contributor to the development of hypertension has been intensively investigated for over 50 years. Evidence from various sources suggests a role for sodium-salt, chloride, calcium, and magnesium. In this article, we will review the evidence supporting a role for each of these electrolytes in human hypertension.
ISSN:0731-5724
DOI:10.1080/07315724.1989.10737972
出版商:Routledge
年代:1989
数据来源: Taylor
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