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

At present the two different mechanisms underlying the hypertriglyceridemia of diabetes are reasonably well defined. The rationale of therapy has grown from this knowledge. One form of hyperlipidemia is due to the hyperinsulinemia which results from the patient's resistance to insulin. The approach to treatment aims to overcome the insulin resistance. In most patients this is done by treating their obesity. The other form of hypertriglyceridemia results from insulin deficiency and is treated by bringing the patient's diabetes under control. There is strongly suggestive evidence that hypertriglyceridemia may be associated with a high risk of atherosclerosis. The reason for treating hypertriglyceridemia in general, and in the diabetic in particular, is to reduce this risk. However, it must be conceded that, at the moment, there is no information about the effect of lower triglyceride levels on the incidence of atherosclerosis. Hence much epidemiologic research is needed before our rationale for treatment can move from the realm of hope to the realm of definite proof. In the mean time an attack on this and the other risk factors is the best way we have to attempt to prevent the major complication of diabetes, atherosclerosis.
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PMID:Hyperlipidemia, atherosclerosis, and diabetes. 20 21

Dietary Cr deficiency may cause the aging-related Cr depletion observed in humans. Such depletion, when it occurs with excessive consumption of sugar and other carbohydrates, may result in glucose intolerance, glycosuria, hyperinsulinemia, and hyperlipidemia. These metabolic disorders could explain why athero-sclerotic diseases are endemic to most Western industrial societies. This review detailed significant current research and findings on the manifestations of Cr deficiency in humans and animal models.
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PMID:Chromium depletion in the pathogenesis of diabetes and atherosclerosis. 33 61

Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in the perifusion system. Islet size was arbitrarily defined as large (greater than 0.45 mm) or small (smaller than 0.12 mm). Protein content and volume (V = 4/3pir3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 +/- 2.4 vs. 1.5 +/- 0.37 microU/islet/min, P less than 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P less than 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P less than 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 +/- 3.3 vs. 4.1 +/- 0.3 pg/microgram protein per minute, P less than 0.05). Arginine produced the same effect on glucagon release (P less than 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
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PMID:Correlation between morphology and function in isolated islets of the Zucker rat. 37 79

Coronary heart disease (CHD) remains an uncommon disorder in the South African Black population. It has been suggested that herein lies an enigma, since it is believed that these people are considerably exposed to the conventional risk factors for CHD. To test this belief I have assessed the exposure of Black people, in time and degree, to the following CHD risk factors: affluence, age, hypertension, hyperlipidaemia, dietary excess, smoking, physical inactivity, diabetes, obesity, hyperuricaemia and hyperinsulinism. Among males only hypertension, and among females only hypertension and obesity, emerged as prominent factors. However, neither of these is significantly atherogenic in the social, nutritional and metabolic milieu in which Blacks generally live, and obesity is a doubtful atherogenic factor, even in westernized populations. It is therefore concluded that the rarity of CHD in Blacks is not enigmatic, but is appropriate to their environmental circumstances.
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PMID:The rarity of coronary heart disease in South African blacks. 69 6

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

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

Blood glucose, free fatty acid and insulin responses to oral glucose and the fasting serum lipids were measured in 3 groups: 32 non-obese (mean age: 47.5 years) and 9 obese (mean age: 84.5 years), male patients with coronary heart disease and 12 non-obese male controls (mean age: 46.5 years). The oral glucose tolerance tests were repeated after 3 years in 16 of the non-obese patients with coronary heart disease. The results were as follows: 1) Glucose tolerance was impaired in 19 of 32 non-obese patients (59.4%). There was a significant correlation between impaired glucose tolerance and hyperlipidemia (hypercholesterolemia and/or hypertriglyceridemia). 2) In obese patients FFA levels at 30, 60, and 120 min after oral glucose administration were significantly elevated and FFA decrease was delayed with a drop to minimum levels at 180 min. 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. In the group of non-obese patients with impaired glucose tolerance, serum insulin levels went up to normal levels, but the peak was delayed. The serum insulin levels in obese patients were significantly higher than those of controls of 0, 60, 120, and 180 min. After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. 4) The metabolic pattern in the non-obese group with impaired glucose tolerance resembled that of "mild diabetes" in delayed response of insulin and FFA, and mild hyperlipidemia. These findings suggest that obesity may contribute to hyperinsulinemia in patients with coronary heart disease and that impaired glucose tolerance observed in patients with coronary heart disease is in part due to "latent diabetes".
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PMID:Glucose tolerance, serum insulin and lipid abnormalities in patients with coronary heart disease. 118 89

Hypercholesterolemia is seen as an important risk factor for coronary artery disease (CAD), as the incidence of CAD is strongly correlated with the level of serum cholesterol in epidemiological studies. However, hypercoagulability and reduced fibrinolytic capacity, often seen in survivors of myocardial infarction, are associated with hypertriglyceridemia (possibly concomitant with low levels of high-density lipoprotein cholesterol) and not with increased levels of total or low-density lipoprotein cholesterol. The important role of thrombogenesis in CAD is supported by the fact that initial high levels of plasma fibrinogen, coagulation factor VII (VIIc), and plasminogen activator inhibitor (PAI-1) are all independent risk factors for CAD or recurrent myocardial infarction as found in multivariate analyses of epidemiological studies. Furthermore, high plasma levels of VIIc and PAI-1 are associated with hypertriglyceridemia, reduced glucose tolerance, overweight, and hyperinsulinemia. The contribution of thrombogenic risk factors to the metabolic cardiovascular syndrome (MCVS) is thus established. Diet intervention is preferable for the normalization of hypercoagulability and hypofibrinolysis associated with MCVS. In familial combined hyperlipidemia, however, and especially with concomitant thromboembolic disease, diet alone is often not sufficient, and drug treatment with anticoagulants and/or lipid-lowering drugs may be necessary.
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PMID:Hypercoagulability and reduced fibrinolysis in hyperlipidemia: relationship to the metabolic cardiovascular syndrome. 128 67

To investigate the hypothesis that insulin resistance plays a role in the etiology of hypertension and hyperlipidemia, we measured serum lipid levels, the fasting glucose/insulin ratio, and the insulin response to oral glucose (GTT) in a group of young obese subjects (n = 21) with hypertension and normal glucose tolerance and in normotensive subjects (n = 36) with normal glucose tolerance, matched for age and body mass index. Leisure time physical activity was evaluated by a questionnaire outlining three levels of physical activities during leisure time. Subjects with hypertension had higher fasting serum insulin (19 +/- 2 v 13 +/- 1 microU/mL, P < .01) and lower fasting glucose/insulin ratio (5.3 +/- 0.2 v 7.1 +/- 0.5 mg/dL/microU/mL, P < .01) than normotensive subjects. Subjects with hypertension had higher peak serum insulin and lower plasma glucose area/insulin area ratio in response to glucose (1.8 +/- 0.2 v 2.4 +/- 0.2 mg/dL/microU/mL, P < .05) than normotensive subjects. Serum total cholesterol, low-density cholesterol, and triglycerides were higher in the obese hypertensive subjects than in obese normotensive ones. Blood pressure correlated with either fasting serum insulin, fasting glucose/insulin ratio, or glucose area/insulin area ratio during GTT. The level of leisure time physical activities was lower in obese hypertensive subjects than in obese normotensive ones. There were significant correlations between the levels of physical activity and the fasting plasma glucose/insulin ratio (r = 0.371, P < .01) or the fasting serum insulin concentration (r = -0.282, P < .05). The study provided evidence that a low level of leisure time physical activity is associated with insulin resistance and resultant hyperinsulinemia, which are the key metabolic abnormalities that link hypertension, obesity, and hyperlipidemia in young subjects.
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PMID:Leisure time physical activity and insulin resistance in young obese students with hypertension. 128 41

A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Hyperinsulinemia has been recognized as a major risk factor for the development of coronary artery disease independent of blood pressure and plasma lipid levels. All these conditions are frequently associated, particularly in aging, a state itself characterized by hyperinsulinemia. This common association has prompted the hypothesis that hyperinsulinemia may be a causative factor rather than the consequence of obesity, diabetes, hypertension, and hyperlipidemia. If that is the case, defining the nature and mechanisms of hyperinsulinemia becomes of primary interest. Insulin resistance is also a striking feature of all of the above mentioned pathologic states. In the presence of a preserved B-cell function, hyperinsulinemia can represent the mechanism designed to overcome the defect in the biological action of the hormone. For instance, there is a clear-cut age-related decline in the body's sensitivity to insulin. In order to compensate for this defect in insulin-mediated glucose metabolism, the B-cell must increase its secretion. On the other hand, a certain degree of insulin resistance can be induced both in animals and man by prolonged euglycemic hyperinsulinemia. Little is known regarding possible primary defects of the B-cell leading to uncontrolled oversecretion of insulin and subsequent insulin resistance. The primary defect, more probably, resides in an alteration of one or more of the steps whereby insulin exerts it own action. In favor of this hypothesis are the observations that insulin resistance segregates in familial clusters and that the first defect found in normoglycemic relatives of insulin-resistant diabetic patients is a reduced transformation of glucose into glycogen. Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration.
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PMID:[Hyperinsulinism. Causes and mechanisms]. 133 21


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