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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that hyperlipidemia is characteristic of growth hormone deficiency in childhood, we have measured serum cholesterol and triglyceride concentrations in 24 euthyroid children with growth hormone deficiency. Although modest elevations of cholesterol and/or triglyceride above the 95th percentile for age, race, and sex were present in 46% of the children studied, the mean (+/- 1 SD) cholesterol of 173 +/- 36 mg/dl and the mean triglyceride of 80 +/- 42 mg/dl were not significantly different from published normal mean values. Administration of human growth hormone for 4 mo to 15 of these subjects did not alter these mean cholesterol and triglyceride values, but did result in a marked improvement in the growth rate. Some individuals (n = 6) with a subnormal growth response to therapy and/or a low serum thyroxine and high serum cholesterol were treated for an additional 4 mo with growth hormone and thyroid hormone together. There was a statistically significant decrement in serum cholesterol in this group. We conclude that modest hyperlipidemia does exist in some children with growth hormone deficiency. Subclinical hypothyroidism may play a role in the hypercholesterolemia of some children, as may growth hormone deficiency itself. Any association of growth hormone and lipid metabolism remains to be clarified.
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PMID:Serum cholesterol and triglycerides in children with growth hormone deficiency. 51 86

Thirty-one growth-hormone-deficient dwarfs were re-examined after a period of 10 to 12 years. These subjects had initially shown glucose intolerance, insulinopenia and hyperlipidemia comparable to those of diabetic patients matched for age and sex, but vascular complications were not present in dwarfs. After 10 years glucose tolerance became progessively more abnormal in dwarfs than could be accounted for by expected deterioration with age, and hyperglycemia after mixed meals remained greater than in control subjects. Serum lipid and serum lipoprotein concentrations were abnormal in over one third of the dwarfs. Despite the metabolic similarity to the diabetic patients, clinical complications of diabetes were absent in dwarfs: retinopathy did not occur, and the prevalence of hypertension and arteriosclerosis was considerably lower in dwarfs than in the diabetic subjects in both study periods. The follow-up data support the hypothesis that growth hormone has at least a supportive role in the pathogenesis of vascular disease in the diabetic state.
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PMID:A follow-up study of vascular disease in growth-hormone-deficient dwarfs with diabetes. 65 62

Significant hypertriglyceridemia, the most common lipid abnormality in renal failure, first occurs when the creatinine clearance falls to 50 ml/min. The prevalence of hypertriglyceridemia continues to rise as creatinine clearance falls further with the highest rate developing at a creatinine clearance less than 10 ml/min. Hypertriglyceridemia is correlated with plasma glucagon levels but not growth hormone or insulin. Plasma cholesterol values remain normal in the face of deteriorating renal function and show no correlation with any of the hormones measured. Although all three hormones became elevated as renal function diminished, none were directly correlated with glomerular filtration rate. There was a distinct decrease in the prevalence of hyperlipidemia after 5 years of maintenance hemodialysis therapy. Plasma growth hormone and glucagon through an effect on plasma triglyceride and plasma insulin by effecting plasma cholesterol may play a role in this decline of hyperlipidemia with duration of hemodialysis.
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PMID:Relationship of plasma lipids to renal function and length of time on maintenance hemodialysis. 70 43

Many alterations in metabolic and endocrine function occur in end-stage renal disease. Glucose intolerance is almost always present with uremia; it improves shortly after institution of regular hemodialysis. Hyperlipidemia (type IV) is prevalent, and atherosclerotic cardiovascular disease causes death in about 50% of patients receiving long-term hemodialysis. Although plasma levels of growth hormone usually are elevated, children with chronic renal failure show growth retardation. The occurrence of thyroid disorders is difficult to determine, since many clinical features of uremia are similar to those of hyperthyroidism and hypothyroidism. The incidence of duodenal ulcer is high, possibly due to high gastrin levels. Sex hormone disturbances are common. Anemia is a constant feature of chronic renal failure; patients usually tolerate it well.
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PMID:Metabolic and endocrine alterations in end-stage renal failure. 71 39

Our study indicates that in renal failure elevated plasma triglyceride can first be detected when the GFR falls to 50 ml/min. Hypertriglyceridemia is the commonest abnormality found and increases further when the GFR falls below 10 ml/min. Plasma cholesterol levels remain normal even at low levels of renal function. Although plasma growth hormone, glucagon, and insulin levels become elevated when renal function diminishes, there is no definite correlation of their levels and GFR. A decreased incidence of hyperlipidemia observed in patients sustained by maintenance hemodialysis for over 5 yrs may in part be due to the triglyceride lowering effect of growth hormone and glucagon and/or the cholesterol lowering effect of insulin.
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PMID:Uremic hyperlipoproteinemia: correlation with residual renal function and duration of maintenance hemodialysis. 91 Mar 86

Destruction of the ventromedial hypothalamic nuclei (VMN) in the weanling rat without injury to the median eminence results in a series of somatic, endocrine, and metabolic changes that are characterized by normal food and water intake but decreased linear growth, normal body weight but increased carcass fat and reduced carcass protein, lean body mass, and water. The endocrine alterations comprise hyperinsulinemia in the face of normoglycemia, hypertriglyceridemia and hypercholesterolemia and reduced growth hormone levels. The metabolic changes include greater oxidation of glucose and incorporation into lipid and reduced palmitate oxidation but increased incorporation into lipid. Weanling rats with VMN lesions are normophagic in absolute terms, relative to body weight and per metabolic unit, but their nocturnal feeding and weight gain cycles are disrupted and their locomotor activity is reduced. The VMN are involved in the long-term control of feeding - as in the mature rat - as shown by intragastric preloading studies and dietary density manipulation, glucose preference tests and intraperitoneal injections with glucose. Hyperinsulinemia and hypertriglyceridemia are present four days after the VMN operation in the presence of subnormal food intake and plasma glucose levels. Manipulations of the fat content of the diet revealed that the hyperlipidemia is of both endogenous and exogenous origin and that lipoprotein lipase is increased; a 48-hour fast reduced the hyperlipidemia to control levels, however. This suggests that weanling VMN rat tissue may have an impaired ability to take up circulating lipid. An increased incorporation of glycerol into lipid may be due to induction of glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per milligram of tissue protein. Glucose oxidation and incorporation into adipose tissue is increased in several tissues in vitro and there is enhanced glucose disappearance from plasma and incorporation into tissue lipids in vivo. These changes develop within a short time after lesion production and persist at least partially up to six months: glucose utilization in liver increases already four hours after the operation whereas it takes 72 hours to commence in adipose tissue. Insulin resistance is not apparent either in vivo or in vitro. The decreased growth hormone levels are not critical to the metabolic changes, nor is the hyperinsulinemia totally necessary. The metabolic changes also appear on several different types of diet and persist with fasting. The latter does not reduce insulin sensitivity of VMN rat tissues, wheras it does so in normal rats. Mature rats developed the same metabolic changes even in the absence of hyperphagia. The metabolic alterations can be blocked by pharmacologic doses of glucocorticoids, but are enhanced by the administration of estrogen...
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PMID:Origin of endocrine-metabolic changes in the weanling rat ventromedial syndrome. 95 Jun 80

A preliminary survey has been completed using manual densitometric technics to determine the mean retinal circulation times in groups of normal controls, offspring to two diabetic parents with normal glucose tolerance (prediabetics), and offspring of two diabetic parents with abnormal glucose tolerance (chemical diabetics). Comparisons of the mean retinal circulation time showed differences between the left eye and right eye in prediabetic and chemical diabetic groups and a sex difference in both normals and prediabetics. In addition, both age and per cent ideal body weight were inversely related to the mean retinal circulation time. The levels of fasting serum cholesterol, triglyceride, and growth hormone, in many instances, also appeared to be inversely related to the mean retinal circulation time. Similarly, the degree of glucose tolerance (determined by the area under the glucose curve above baseline) was significantly inversely related to the mean retinal circulation time. The mean retinal circulation time adjusted for per cent ideal weight was analyzed separately for both right eye and left eye, and a significantly shorter mean retinal circulation time was noted, particularly in males, for prediabetics than for normal controls and for chemical diabetics than for both prediabetics and normals. Analysis of the mean retinal circulation time adjusted for age showed similar differences. It is postulated that the genetic prediabetic state with or without glucose intolerance might be associated with significant alterations of mean retinal circulation time independent of age and per cent ideal weight. It is also suggested that a number of potentially meaningful interrelationships between the degree of glucose intolerance and/or hyperlipidemia might exist and should be further quantified.
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PMID:Mean retinal circulation time as determined by fluorescein angiography in normal, prediabetic, and chemical-diabetic subjects. 97 94

A single s.c. injection (10 mg/100 g bw of alloxan) was given to nonarteriosclerotic, virgin, Sprague--Dawley rats and to breeder rats with preexisting arteriosclerosis, hyperlipidemia and hyperglycemia. All of the animals promptly developed severe diabetes with ketosis, hyperglycemia, and hyperlipidemia. Insulin therapy was deliberately withheld. Mortality was high. Seven days later one group was subjected to hypophysectomy and 30 days later, all of the animals were autopsied. The diabetes + hypophysectomy animals maintained their body weight better, did not have hypertrophied adrenal glands, showed the least elevation of serum enzymes, e.g., CPK, SGOT, SGPT and LDH, less hyperlipidemia and hyperglycemia and reduced corticosterone production than the animals with untreated severe diabetes. Despite the relative amelioration of metabolic derangements prognostic of cardiovascular degenerative changes, the diabetes + hypophysectomy animals manifested extensive renovascular damage and the breeder rats with pre-existing arteriosclerosis showed definite exacerbation of their arterial disease in response to the severe alloxan diabetes regardless of hypophysectomy. It is suggested that although hypophysectomy may alleviate certain metabolic derangements attributed to growth hormone, ACTH and adrenal steroids, the angiopathic damage proceeds inexorably.
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PMID:Effects of hypophysectomy on alloxan-diabetic, arteriosclerotic, breeder vs. non-arteriosclerotic, virgin rats. 98 94

Plasma cholesterol, triglyceride and apolipoprotein B were measured in healthy women during pregnancy. Hyperlipidaemia was most marked in the third trimester of pregnancy, but the increases in cholesterol, triglyceride and apolipoprotein-B were not identical (14, 74 and 36%, respectively). The increase in plasma cholesterol was due to a progressive rise in very low density (VLDL) and low density (LDL) lipoproteins. There was a change in composition and size of both VLDL and LDL, demonstrated by a reduction in the ratio of cholesterol to apolipoprotein-B and altered properties of both lipoproteins on polyacrylamide gradient gel electrophoresis. It is difficult to explain these changes but they did not appear to be related to growth hormone, oestrogens or progestogens.
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PMID:Plasma lipoproteins in pregnancy. 100 19

Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sex-matched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the proportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology.
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PMID:Studies on the nature and causes of hyperlipidaemia in uraemia, maintenance dialysis and renal transplantation. 110 47


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