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

Mandibuloacral dysplasia (MAD) is a syndrome with onset in midchildhood. The predominant characteristics of MAD include flexion contractures; mandibular hypoplasia; loss of body fat; atrophic, speckled skin; and progressive osteolysis of the clavicles. We studied three males with MAD. Each had lipodystrophy of the extremities, with sparing of the face and neck. All had moderate hyperlipidemia. In response to oral glucose, each had a diabetic response, with peak insulin levels between 2870 and 22,960 pmol/L. Insulin-stimulated glucose disposal was determined in two patients with MAD. At an insulin infusion rate of 120 mU/m2 per minute, glucose disposal was less than 25% of that measured at similar levels of insulinemia in nondiabetic control subjects, indicating marked insulin resistance in patients with MAD. The insulin resistance occurred without obesity, excessive levels of counterregulatory hormones, or anti-insulin-receptor antibodies. We suggest that MAD is a previously undescribed form of lipodystrophic insulin-resistant diabetes mellitus.
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PMID:Severe insulin resistance and diabetes mellitus in mandibuloacral dysplasia. 173 53

Diabetes mellitus is one of the most common medical problems in elderly patients. There is a strong rationale for therapy in most patients with diabetes, even those who are asymptomatic. Family physicians should be aware of several age-associated differences in the management and treatment of diabetes in older patients. For elderly patients, dietary modifications may include an increase in the percentage of carbohydrates and a decrease in the percentage of fat. For obese patients, dietary therapy should also emphasize a decrease in overall calories. Oral hypoglycemic agents are generally used as the initial drug therapy. Insulin therapy should be instituted when oral agents fail to reduce the blood glucose level, when the blood glucose level is very high and in other special circumstances. A careful choice of medications for other common problems associated with diabetes, such as hypertension, hyperlipidemia and peripheral neuropathy, is also essential.
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PMID:Treatment of diabetes in the elderly. 187 33

Elevated fasting insulin is an independent risk factor for hyperlipidemia, hypertension, and cardiovascular disease, but determinants of insulin other than age and body mass remain poorly described. Potentially modifiable factors associated with insulin were identified by correlating anthropometric, dietary and physical activity data in the CARDIA cohort of 2643 black and 2472 white men and women aged 18-30 years. Insulin was positively correlated with serum glucose, body mass index (BMI), skinfold thickness, waist/hip ratio and sucrose intake, and negatively correlated with heavy physical activity score, treadmill exercise duration, and magnesium intake (each p less than 0.01). After adjustment for other covariates, the positive association of insulin with waist/hip ratio, skinfold thickness, and sucrose intake remained in the group as a whole, as did the negative associations with magnesium and treadmill duration. These relationships provide insight into potentially modifiable factors affecting insulin levels, and should be considered in interpreting associations between insulin levels and cardiovascular disease.
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PMID:Correlates of fasting insulin levels in young adults: the CARDIA study. 203 62

Juvenile coho salmon (Oncorhynchus kisutch) were placed on five dietary regimes: fed 1 week, fasted 1 week, fed 3 weeks, fasted 3 weeks, and fasted 1 week/refed 2 weeks. Plasma levels of glucose, fatty acids, insulin, glucagon, and glucagon-like peptide (GLP) and the activities of key metabolic enzymes were determined. Plasma glucose levels in the fed control groups were 98.4 +/- 3.4 (SEM) and 104.8 +/- 4.7 mg/dl at 1 and 3 weeks, respectively. Plasma glucose in the fasted 1 week group was significantly elevated to 128.8 +/- 9.2 mg/dl. Animals fasted 3 weeks or fasted 1 week/refed 2 weeks displayed plasma glucose levels similar to those of fed animals. Fasted groups possessed significantly less liver glycogen than fed or fasted/refed groups. Plasma fatty acids were elevated only after 3 weeks of fasting (from 0.39 +/- 0.04 microEq/ml to 0.61 +/- 0.06 microEq/ml). This response was reflected in elevated liver lipase activity (from 6.02 +/- 0.44 nmol fatty acid released/hr/mg protein to 14.22 +/- 0.90 units). No significant alterations in liver lipogenesis, assessed by glucose-6-phosphate dehydrogenase activity and by 3H2O incorporation into fatty acids, were observed. Gluconeogenic flux, determined indirectly through kinetic parameters of pyruvate kinase, was enhanced in animals fasted 3 weeks and in animals recovering from a 1-week fast. Plasma insulin levels were highest in fed groups (7.7 +/- 2.3 and 5.9 +/- 1.4 ng/ml at 1 week and 3 weeks, respectively) and were significantly depressed in fasted groups. Plasma levels of glucagon and GLP were also depressed in fasted groups. These results indicate that plasma glucose levels are maintained in salmon during fasting and that fasting-induced hyperlipidemia is mediated by lipolytic enzyme activity. Insulin, glucagon, and GLP may interact with these enzyme systems to coordinate nutritional metabolism of fish.
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PMID:Effects of nutritional state on in vivo lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 205 44

Insulin resistance is one of pathogenic factors for non-insulin-dependent diabetes mellitus (NIDDM). Pioglitazone (5-[4-[2-(5-ethyl-2-pyridyl)-ethoxy]benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) is a promising candidate to lower hyperglycemia by reducing insulin resistance. The genetically obese-hyperglycemic rats. Wistar fatty, were used to test the action of pioglitazone, because they develop severe insulin resistance in the peripheral tissues (muscle and adipose tissue) and liver. Pioglitazone administered orally (0.3-3 mg/kg/d for 7 days) dose dependently reduced hyperglycemia, hyperlipidemia, and hyperinsulinemia in male fatty rats. Pioglitazone improved glucose tolerance and augmented the glycemic response to exogenous insulin and clearance of plasma triglyceride. These effects on glucose and lipid metabolism seem to be due to increased insulin sensitivity and responsiveness in the peripheral tissues, because pioglitazone increased insulin-stimulated glycogen synthesis and glycolysis in the isolated soleus muscles, and insulin-stimulated glucose oxidation and lipogenesis in adipocytes. The latter effects were not accompanied by any changes in insulin binding. The actions of insulin mimickers (vanadate and vitamin K5), which act on the post-insulin binding sites, on these metabolic events were also potentiated by pioglitazone. These findings suggest that pioglitazone can improve glucose and lipid metabolism by reducing insulin resistance on the post-binding system. Therefore, pioglitazone may be efficacious for treating human NIDDM.
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PMID:Effects of pioglitazone on glucose and lipid metabolism in Wistar fatty rats. 218 19

Atherosclerosis is the most prevalent long-term diabetic complication. The increased mortality and morbidity in diabetics caused by atherosclerosis has been related to the frequent occurrence of hyperlipidaemia in diabetes. Insulin regulates many processes in lipid metabolism via control of enzyme activity and receptor binding. It is important to establish a precise diagnosis of the lipid abnormalities before commencing treatment. The treatment begins with control of blood glucose, followed by dietary treatment of hyperlipidaemia. Hypolipidaemic drugs are first introduced when the dietary response is unsatisfactory. Optimal therapy with antidiabetic drugs should precede hypolipidaemic drug therapy.
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PMID:[Hyperlipidemia in diabetes mellitus. Pathogenesis, diagnosis and drug therapy--a review]. 240 21

A new congenic strain of rat, the SHR/N-corpulent, provides a good model for noninsulin-dependent diabetes and was used in the present study. Corpulent rats as compared to their lean littermates are obese, hyperlipidemic, and severely hyperinsulinemic, and show an age-dependent loss of glucose tolerance. Mild fasting hyperglycemia is seen only in corpulent rats fed sucrose. Since dietary sucrose is more lipogenic than starch and since insulin and glucagon are involved in lipid and carbohydrate metabolism, we studied the effect of the type of dietary carbohydrate on insulin and glucagon levels and their receptors in lean and corpulent SHR/N rats. A significant phenotypic effect was observed (corpulent greater than lean) on plasma levels of triglyceride, cholesterol, and insulin. Dietary sucrose increased these parameters in corpulent rats but not in lean rats. Insulin and glucagon binding to liver plasma membranes was lower in corpulent rats than in lean; decreases were due to fewer receptors without a significant change in affinity. Thus, in corpulent rats, in addition to hyperinsulinemia, fewer glucagon receptors and their failure to be regulated by plasma glucagon levels appear to contribute to the hyperlipidemia. Furthermore, the hyperglycemia observed in sucrose-fed corpulent rats may be due to extreme resistance to insulin despite lower plasma glucagon and fewer glucagon receptors.
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PMID:Effect of dietary carbohydrates on insulin and glucagon receptors in a new model of noninsulin-dependent diabetes-SHR/N-corpulent rat. 255 55

A catabolic and hypolipemic effect of glucagon has been described in normal animals. We therefore studied the role of glucagon in genetically obese, hyperlipemic rats. Twelve genetically obese hyperlipemic LA/N-cp/cp (corpulent) rats and 12 lean littermates were fed either 54% starch or 54% sucrose for 12 weeks. Plasma glucagon and insulin levels and glucagon and insulin binding to liver membranes were measured. Comparing all corpulent and lean animals regardless of diet, a significant (P less than 0.0001) phenotypical effect (cp/cp greater than lean) was observed in plasma insulin levels (464 +/- 54 vs 70.3 +/- 7.6 muu/ml, mean +/- SEM). Insulin binding (2.68 vs 16.1%/50 micrograms protein) and glucagon binding (25.6 vs 47.3%/50 micrograms protein) were both significantly lower (P less than 0.0001) in corpulent rats as compared to their lean littermates. Sucrose feeding had marginal effect on plasma insulin or insulin binding. It, however, decreased glucagon binding in corpulent rats but not in their controls. A significant negative correlation was observed between plasma insulin and insulin binding, while a positive correlation was seen for plasma glucagon and glucagon binding. A significant negative correlation was observed between plasma glucagon and lipogenic enzymes (glucose-6-phosphate dehydrogenase and malic enzyme) in liver and between glucagon binding and these enzymes. We propose that in these genetically obese rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target cells may be an important contributor to the hyperlipemia and obesity. A further decrease in glucagon binding in rats fed sucrose indicates that sucrose, per se, may be an additional contributory factor.
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PMID:Genetic obesity and dietary sucrose decrease hepatic glucagon and insulin receptors in LA/N-corpulent rats. 300 53

Obese Zucker rats are hyperlipemic and mildly hyperglycemic. Because insulin and glucagon are involved in lipid and carbohydrate metabolism and they act via their receptors, we investigated the role of insulin and glucagon receptors in obese and lean female Zucker rats. Because dietary sucrose is more lipogenic than starch, we also studied the effect of dietary carbohydrates on the receptors. Significant phenotypic effect (obese greater than lean) was observed on plasma levels of glucose, triglyceride and insulin. Binding of insulin and glucagon to liver plasma membranes was significantly lower in obese rats than in lean rats. Lower insulin binding was due to a lower number of receptors as well as a lower affinity, whereas the lower glucagon binding was due only to a lower receptor number. Insulin binding in lean rats but not in obese rats was lower in sucrose-fed than in starch-fed rats. Diet had no effect on glucagon binding. We propose that in obese Zucker rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target tissues may be an important contributor to the hyperlipemia and obesity.
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PMID:Effect of dietary carbohydrates on glucagon and insulin receptors in genetically obese female Zucker rats. 303 87

The standard treatment of NIDDM consists of diet, oral hypoglycaemic agents and, mostly as a last resort, insulin. Indications for insulin therapy cannot be generalized for the whole population of NIDDM patients. The defined objectives of therapy for the individual patient will determine the choice and intensity of therapy. These will usually be either a relief of hyperglycaemic symptoms in the elderly patient or normoglycaemia, as in the insulin-dependent diabetic patients, in order to prevent acute and chronic complications. Primary insulin treatment is advisable in patients with hyperglycaemic symptoms and fasting blood glucose levels above 15 mmol/l, as in these patients the major defect will be insulin deficiency rather than insulin resistance. The correction of long lasting hyperglycaemia partly restores insulin sensitivity and B cell function, thereby allowing sequential reduction of insulin dosage. When metabolic control can be sustained with low insulin dosages some of these patients may later respond well to oral hypoglycaemic agents or to diet alone. In the management of non-insulin-dependent diabetic patients it is of great importance to recognize in time when treatment with oral hypoglycaemic agents fails. Insulin therapy should not be withheld on the presumption that it will cause weight gain and will promote development of macrovascular disease. Weight gain can be reduced by adequate dietary counselling and the level of macrovascular risk factors reduces with improved metabolic control. In this context also it should be realized that the correction of hypertension, hyperlipidaemia and the cessation of cigarette smoking is probably of equal importance. Insulin therapy regimens which have been used in non-insulin-dependent diabetic patients have been the same as prescribed for insulin dependent patients. When considering the fact that hepatic overproduction of glucose is the major determinant of fasting blood glucose level and that postprandial glycaemic excursions are superimposed on this level it seems reasonable to aim for normalization of the basal hepatic glucose production. A bedtime injection of an intermediate or long acting insulin can be used for this aim. Other therapeutical approaches which have been studied recently are the use of combinations of insulin and oral hypoglycaemic agents and the use of proinsulin as an alternative for intermediate acting insulin. Before these forms of therapy can be advocated long-term clinical studies are necessary to define their therapeutic role.
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PMID:Insulin treatment of non-insulin-dependent diabetes mellitus. 307 3


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