Type II Hyperlipoproteinemia159, 192 193 194 195 196 General Definitions By the Type II lipoprotein pattern we mean an increase in the concentration of lipoproteins that have discrete β mobility b

Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders

Nutrition is one of the main regulators of circulating IGF-I. In humans, serum IGF-I concentrations are markedly lowered by energy and/or protein deprivation. Both energy and proteins are critical in the regulation of serum IGF-I concentrations. Indeed, after fasting, optimal intake of both energy and protein is necessary for the rapid restoration of circulating IGF-I. We believe, however, that in adult humans energy may be somewhat more important than protein in this regard. While the lowest protein intake is able to increase IGF-I in the presence of adequate energy, there is a threshold energy requirement below which optimal protein intake fails to raise IGF-I after fasting. When energy intake is severely reduced, the carbohydrate content of the diet is a major determinant of responsiveness of IGF-I to GH. The essential amino acid content of the diet is also critical for the optimal restoration of IGF-I after fasting, when protein intake is reduced. The exquisite sensitivity of circulating IGF-I to nutrients, the nycthemeral stability of its concentrations and its relative short half-life constitute the basis for its use as a marker of both nutritional status and adequacy of nutritional rehabilitation. For these indications, IGF-I measurement is more sensitive and more specific than measurement of the other nutrient-related serum proteins (albumin, prealbumin, transferrin, retinol-binding protein). Animal models have been developed to investigate the mechanisms responsible for the nutritional regulation of IGF-I. There is no doubt that many mechanisms are involved (Fig. 12). Decline of serum IGF-I in dietary restriction is independent of the diet-induced alterations in pituitary GH secretion. The role of the liver GH receptors is dependent on the severity of the nutritional insult. In severe dietary restriction (fasting), a marked decrease of the number of somatogenic receptors supports the role of a receptor defect in the decline of circulating IGF-I. In contrast, in less severe forms of dietary restriction (protein restriction), the decline of IGF-I results from a postreceptor defect in the GH action at the hepatic level. Nutritional deprivation decreases hepatic IGF-I production by diminishing IGF-I gene expression. Decline in IGF-I gene expression is mainly caused by nutrient deficiency and less importantly by the nutritionally induced hormonal changes (insulin and T3). Diet restriction also increases the clearance and degradation of serum IGF-I through changes in the levels of circulating IGFBPs.(ABSTRACT TRUNCATED AT 400 WORDS)

Nutritional Regulation of the Insulin-Like Growth Factors*

Multivalent feedback regulation of HMG CoA reductase, a control mechanism coordinating isoprenoid synthesis and cell growth

Metabolism and function of coenzyme Q

We studied the metabolic effects of stearic acid (18:0) on plasma lipoprotein levels in 11 subjects during three dietary periods of three weeks each. The three liquid-formula diets, which were used in random order, were high in palmitic acid (16:0), stearic acid, and oleic acid (18:1), respectively. Caloric intakes were the same during the three periods. As compared with the values observed when the subjects were on the high-palmitic-acid diet, plasma total cholesterol decreased by an average of 14 percent during consumption of the high-stearic-acid diet (P less than 0.005) and by 10 percent during consumption of the high-oleic-acid diet (P less than 0.02). Low-density lipoprotein cholesterol levels fell by 21 percent in subjects on the high-stearic-acid diet (P less than 0.005) and by 15 percent in subjects on the high-oleic-acid diet (P less than 0.005). No significant differences were observed in the plasma levels of triglycerides or high-density lipoprotein cholesterol among the three diets. Measurements of the intestinal absorption of palmitic, stearic, and oleic acids revealed essentially complete absorption of each during the three dietary periods. The oleic acid content of plasma triglycerides and cholesteryl esters increased significantly during the high-stearic-acid period, suggesting that stearic acid is rapidly converted to oleic acid. We conclude that stearic acid appears to be as effective as oleic acid in lowering plasma cholesterol levels when either replaces palmitic acid in the diet.

Effect of Dietary Stearic Acid on Plasma Cholesterol and Lipoprotein Levels

Plasma somatomedin and growth hormone values in children with protein-calorie malnutrition.

Nutrition-endocrine interrelationships in the control of fat transport in man.

Prevention by hypothermia of paradoxical calcium necrosis in cardiac muscle.

IN addition to being a substrate for protein synthesis in the body, dietary tryptophan is metabolized to at least two physiologically important compounds, nicotinic acid and serotonin, via the intermediates outlined in Figure 1. The major urinary metabolites of these two compounds are respectively N-methylnicotinamide (and its 6-pyridone)1 and 5-hydroxyindoleacetic acid (5-HIAA).2 In this paper we wish to report a reduced rate of 5-HIAA excretion in the urine of patients with chronic alcoholism. Since the rate of N-methylnicotinamide formation from tryptophan was unchanged, the reduced 5-HIAA excretion may signify a defective conversion of tryptophan to serotonin in these addicts. Methods The . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM196012082632304?listPDF=true

Evidence for a Defect in Tryptophan Metabolism in Chronic Alcoholism

Publisher Summary This chapter discusses Vitamin K and γ-Carboxyglutamate Biosynthesis. Long periods of time may elapse between the discovery of a given vitamin deficiency disease, the isolation and structural analysis of the vitamin, and the final elucidation of its metabolic function. It is now established that vitamin K is part of a membrane bound carboxylase system and participates in the posttranslational carboxylation of selected peptide-bound glutamate residues in a number of vitamin K-dependent proteins. The requirements of this carboxylase system are reduced vitamin K, carbon dioxide, oxygen, and a suitable peptide substrate. The precise mechanism of the carboxylase reaction and the biochemical role of vitamin K are still unknown. It is now clear that vitamin K is also involved in an electron transport system in microsomes of mammalian organisms carrying out peptide-bound glutamate carboxylation. The chain involves NADH, vitamin K, and presumably oxygen as a terminal electron acceptor. The energy generated in this electron transport system is coupled in an as yet undetermined way to CO 2 fixation in glutamate. The intuitive belief that vitamin K should be involved in an electron transport system in expressing its procoagulant activity has been vindicated by recent work.

Robert E. Olson

Papers

Plasma somatomedin and growth hormone values in children with protein-calorie malnutrition.

Nutrition-endocrine interrelationships in the control of fat transport in man.

Prevention by hypothermia of paradoxical calcium necrosis in cardiac muscle.

Evidence for a Defect in Tryptophan Metabolism in Chronic Alcoholism

Vitamin K and gamma-carboxyglutamate biosynthesis.