UMLS:C0020473 - FACTA Search

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Query: UMLS:C0020473 (hyperlipidemia)
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We have evaluated the suitability of different rat models for the study of effects of antihypertensives on cardiovascular and metabolic complications of diabetes mellitus and hypertension. IDDM was induced in Wistar and spontaneously hypertensive (SH) rats by single tail vein injection of STZ (45 mg/kg, i.v.). Neonatal STZ-diabetes (nSTZ) was induced by administering STZ, 70 mg/kg (i.p.) to 5 day old Wistar rat pups. DOCA-hypertension was induced in Wistar and STZ-diabetic rats using deoxycorticosterone acetate (DOCA, 5 mg/kg, s.c.) and NaCl (2%) in drinking water. Intravenous injection of STZ produced cardinal signs of diabetes mellitus including hyperglycemia, loss of body weight, polyphagia and polydipsia. STZ-diabetic rats also showed hyperlipidemia and hypoinsulinemia. STZ-treated rats developed hypertension and bradycardia. nSTZ rats were found to have mild hyperglycemia and were hypertensive and hyperinsulinemic. The OGTT and ITT revealed that nSTZ rats are insulin resistant. SH rats were also found to be hyperinsulinemic and hypertensive. Although, these rats were found to be insulin resistant, they did not demonstrate hyperglycemia. DOCA-treated STZ-diabetic rats were found to have milder hyperglycemia when compared to STZ-diabetic rats not treated with DOCA. Although, DOCA treatment was not found to alter serum levels of glucose and insulin, results of OGTT revealed enhanced glucose disposal in DOCA-treated Wistar rats, suggesting that DOCA probably produces some effect on glucose homeostasis in rats. The present data also suggest that STZ-diabetic rat may be considered a suitable model for IDDM. On the other hand, nSTZ and SH rats were hyperinsulinemic and insulin resistant and may be used as models to study insulin sensitivity. DOCA-hypertensive rat may not be a suitable model for studying the effects of various drug interventions on glucose homeostasis and insulin sensitivity as DOCA itself appears to influence these factors.
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PMID:Comparative evaluation of different rat models with co-existing diabetes-mellitus and hypertension. 1084 25

Hypertension is often associated with diabetes mellitus. Its physiopathology is different when it's a question of type 1 or type 2 diabetes mellitus. In the case of type 1 diabetes mellitus, hypertension is often the result of a underlying nephropathy. In the case of type 2 diabetes mellitus, hypertension is more often essential and it lies within a plurimetabolic syndrome and insulin resistance context. In all cases, hypertension worsens the patients' prognostics, increasing the risk of macrovascular and microvascular complications. The optimal blood pressure control allows to limit their evolution. It is necessary to fight against all cardiovascular risks like sedentary lifestyle, obesity, tabacco or hyperlipemia. ANAES recommends a blood pressure control lower or equal to 140/80 mmHg. In type 1 diabetes mellitus, the angiotensin converting enzyme inhibitors (ACE) are the first recommended treatment because of their action in case of nephropathy. In type 2 diabetes mellitus, besides ACE, diuretics. beta-blockers can be used in first line. Often, therapeutic associations are necessary.
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PMID:[Hypertension and diabetes]. 1119 Feb 92

Diabetes mellitus is, as compared with the non-diabetic population, associated with a much higher mortality of ischaemic heart disease and other cardiovascular diseases. In this risk participates in a major way also diabetic dylipidaemia. The latter is characterized in particular by hypertriglyceridemia which reflects the increase of VLDL and IDL lipoproteins. Elevated and prolonged postprandial lipaemia participates in the development of qualitative lipoprotein changes. Highly athergenic "small dense LDL" are formed which are liable to an oxidative modification and are then in an unregulated manner taken up in the vascular wall. Reduction of HDL-cholesterol and a change in the different HDL sub-populations leads then to a deteriorated reverse cholesterol transport. Type 2 diabetes mellitus is associated with dyslipidaemia in the majority of patients even under conditions of satisfactory compensation of diabetes, in particular during the postprandial stage. On the other hand, in type 1 diabetes the lipid values usually become normal when the blood sugar level becomes normal, however qualitative changes of lipoproteins frequently persist. Increased glycation and oxidation of lipoproteins is a common sign of both types of diabetes. For prevention of cardiovascular complications treatment of diabetic dyslipidaemia is at least equally important as efforts to achieve optimal compensation of diabetes. Successful treatment of diabetic dyslipidaemia includes efforts to achieve compensation of diabetes, optimation of body weight, increase of physical activity, modification of diet, treatment of other secondary causes of hyperlipidaemia, and if these provisions are not successful, pharmacological hypolipidaemic treatment. The risk of macrovascular complications is so high in diabetics that according to recent knowledge it is not necessary to differentiate between primary and secondary prevention but aggressive treatment is necessary to achiebe target values of total cholesterol < 5.0 mmol/l and LDL-cholesterol < 3.0 mmol/l. Triglycerides > 2 mmol/l and HDL-cholesterol < 1 mmol/l are signs of a high cardiovascular risk. Optimation of the whole lipid profile is ideal.
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PMID:[Dyslipoproteinemia and diabetes mellitus]. 1134 47

Diabetic Nephropathy is one of the microvascular complications associated with type 1 diabetes mellitus with a major portion of the excess morbidity and mortality. In order to avoid or at least delay its onset we should detect a very small amount of proteins in the urine (between 15-20 and 200 micrograms/min.) that is a strong predictor of those likely to progress to overt nephropathy. This detection can be obtained evaluating an overnight sample of urine and suggest preventives interventions. such as intensive diabetes management and angiotensin converting enzyme inhibition (ACEi). Furthermore, associated risk factors should be prevented or treated (hypertension, retinopathy, hyperlipidemia and smoking).
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PMID:[Practical considerations on screening for microalbuminuria in children and adolescents with type 1 diabetes]. 1142 22

In this review we present the agents that are in use in the treatment of type 2 diabetes. Sulfonylureas of the 1st and 2nd generation increase insulin secretion but can induce hyperinsulinemia and sometimes prolonged hypoglycemia. Glimepiride is a new 3rd generation sulfonylurea with some advantages over the other members of this group, such as a lower risk of hypoglycemia, no interaction with cardiovascular KATP-channels and a possibility that it may increase insulin sensitivity. There are also newer insulin secretagogues (such as neteglinide and repaglinide) with a rapid onset of action on the beta-cell, therefore inducing a more physiological profile of insulin secretion during meals. The category of insulin sensitizers includes metformin and thiazolidinediones. Metformin effectively reduces hyperglycemia, hyperlipidemia and macroangiopathy in patients with type 2 diabetes. This agent increases the sensitivity of the liver and peripheral tissues to insulin and, therefore, it could be considered as a drug of choice for the prevention of type 2 diabetes. Thiazolidinediones (rosiglitazone and pioglitazone) increase the sensitivity of the tissues to insulin. This mechanism of action makes them powerful therapeutic tools for the treatment of type 2 diabetes (and possibly other insulin resistant states) either alone or in combination with other oral agents. The category of agents that interfere with the absorption of glucose and lipids includes alpha-glucosidase inhibitors (acarbose and miglitol) and lipase inhibitors (or-listat). alpha-Glucocidase inhibitors improve the time relationship between plasma insulin and glucose increases after a meal. Therefore, these agents may be used in the treatment of patients with type 2 diabetes, either alone at a very early stage of this disease (when insulin secretion is still adequate), or in combination with insulin secretagogues. alpha-Glucosidase inhibition may also prove useful as a supplement to insulin therapy in patients with type 1 diabetes mellitus. The inhibitor of gastrointestinal lipase orlistat may prove a useful adjunct to hypocaloric diets in patients with type 2 diabetes and obesity.
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PMID:Oral hypoglycemic agents: insulin secretagogues, alpha-glucosidase inhibitors and insulin sensitizers. 1146 May 77

The prevalence of type 2 diabetes is rising in all Westernized societies. Presumably as a consequence of diminishing cardiovascular mortality, end-stage renal failure (ESRF) in patients with diabetes (mostly type 2) as a co-morbid condition has risen dramatically in the past decade. This constellation has become the single most common cause of ESRF in most countries. Such an epidemiological trend is particularly regrettable, since in uraemic diabetic patients, medical rehabilitation and survival are remarkably poor. Recent studies indicate that an interplay between genetic predisposition and factors, some of them susceptible to intervention, such as hyperglycaemia, blood pressure, smoking, age, gender and ethnicity, predispose to the development and progression of nephropathy. It has also become clear that trace albuminuria ('microalbuminuria') provides unique opportunities to recognize incipient renal involvement early on, although it is less specific in type 2 as compared with type 1 diabetes. Factors that promote progression include hypertension, proteinuria, smoking, glycaemic control and, less certainly, dietary protein intake and hyperlipidaemia. Cumulating evidence indicates that early intervention delays progression of nephropathy. The most important strategies to combat the medical catastrophe of increasing numbers of diabetic patients with ESRF include: (i) prevention of diabetes (mainly type 2); (ii) glycaemic control to prevent onset of renal involvement; and (iii) meticulous antihypertensive treatment to avoid progression of nephropathy.
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PMID:Renal disease in type 2 diabetes. 1150 79

Almost all major causes of ill-health and premature death in human societies worldwide - including cancer, cardiovascular disease, diabetes and many infectious diseases - are, at least in part, genetically determined. Typically, risk of succumbing to one of these illnesses is thought to depend on both the individual repertoire of variation within a number of key susceptibility genes and the history of exposure to relevant environmental factors. For many of these conditions, the molecular basis of disease pathogenesis remains obscure. This represents a major obstacle to development of improved, rational strategies for disease treatment, prevention and eradication. It is easy therefore to appreciate the importance attached to efforts to deliver more comprehensive understanding of the molecular basis of disease pathogenesis. Nor is it hard to understand that identification of major susceptibility genes should highlight those components of molecular machinery that are critical for the preservation of normal health. The benefits promised are great, but progress to gene identification in multifactorial traits has been rather disappointing to date. Why is this? This review aims to answer this question by describing current and future approaches to gene discovery in multifactorial traits. The examples quoted will mostly relate to type 2 diabetes, but the issues and approaches are generic, and apply equally to other multifactorial traits in the endocrine and metabolic arena - type 1 diabetes; obesity; hyperlipidaemia; autoimmune thyroid disease; polycystic ovarian syndrome - and beyond.
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PMID:Susceptibility gene discovery for common metabolic and endocrine traits. 1185 95

Stabilized rice bran (SRB), a source of complex carbohydrates, tocols, gamma-oryzanols, and polyphenols, was treated with carbohydrases and heat to yield two fractions, rice bran water solubles (RBWS), and rice bran fiber concentrates (RBFC). Stabilized rice bran and its fractions were fed for 60 days to insulin-dependent and noninsulin-dependent diabetes mellitus (IDDM = Type I and NIDDM = Type II) subjects to determine possible effects on serum hemoglobin, carbohydrate and lipid parameters. The Type I subjects (n = 22, 26, and 20) fed Stabilized rice bran, rice bran water solubles, and rice bran fiber concentrates plus AHA Step-1 diet reduced glycosylated hemoglobin 1%, 11%, and 10%, respectively. The fasting serum glucose levels were also reduced significantly (P < 0.01) with stabilized rice bran (9%), rice bran water solubles (29%), and rice bran fiber concentrates (19%).The Type II subjects (n = 31, and 26) fed rice bran water solubles and rice bran fiber concentrates plus AHA Step-1 diet had decreased levels of glycosylated hemoglobin (15% and 11%) and fasting glucose (33% and 22%; P < 0.001), respectively. Serum insulin levels were increased (4%) with rice bran water solubles in both types of diabetes. The reduction of glycosylated hemoglobin and a slight increase in insulin levels indicate that consumption of rice bran water solubles can control blood glucose levels in human diabetes. Serum total cholesterol, LDL-cholesterol, apolipoprotein B, and triglycerides levels were reduced with rice bran fiber concentrates in the Type I (10, 16, 10, 7%) and Type II groups (12, 15, 10, 8%), respectively. These results indicate that rice bran water solubles significantly reduces hyperglycemia (P < 0.01), whereas rice bran fiber concentrates reduces hyperlipidemia (P < 0.05) in both types of diabetes. Therefore, these natural products can be used as nutritional supplements for the control of both types of diabetes mellitus in humans.
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PMID:Effects of stabilized rice bran, its soluble and fiber fractions on blood glucose levels and serum lipid parameters in humans with diabetes mellitus Types I and II. 1189 82

We sought to investigate the ability of biphasic insulin aspart 30 (BIAsp 30) to control postprandial hyperglycemia and hyperlipidemia in a meal-test comparison with biphasic human insulin 30 (BHI 30). In this randomised crossover trial, 50 patients with type 1 diabetes (mean age, 35.7 +/- 9.4 years; body mass index [BMI], 24.0 +/- 2.6 kg/m(2); HbA(1c), 8.6% +/- 1.1%) were studied on 3 separate days, where the following treatments were given in random order: BIAsp 30 injected immediately before a standard breakfast, BHI 30 injected 30 minutes before breakfast (BHI 30(t=-30)), and BHI 30 injected immediately before breakfast (BHI 30(t=0)). The dose was 0.40 U/kg for all 3 treatments. BIAsp 30 reduced the area under the baseline adjusted 4-hour postprandial serum glucose curve (AUC(0-4h)) by 23% compared with BHI 30(t=0) (P <.0001) and by 9% compared with BHI 30(t=-30) (P =.013). Maximum serum glucose concentration (C(max)) was lower for BIAsp 30 compared with BHI 30(t=0) (14.0 +/- 2.4 v 16.5 +/- 2.8 mmol/L, P <.0001), and time to maximal serum glucose concentration (t(max)) was approximately 20 minutes shorter for BIAsp 30, irrespective of timing of BHI 30 injection (P <.0001). There were no significant differences among the 3 treatments with respect to postprandial levels of free fatty acids or triglycerides. The pharmacokinetic results were consistent with the above observations, ie, significantly larger insulin AUC(0-4h), higher C(max) and shorter t(max) were observed for BIAsp 30 compared with BHI 30, irrespective of timing of BHI 30 injection. We conclude that postprandial glycemic control was more effective with BIAsp 30 than with BHI 30, irrespective of timing of BHI 30 injection.
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PMID:Postprandial glycemic control with biphasic insulin aspart in patients with type 1 diabetes. 1207 38

Oxidative modification of lipoproteins in vessel walls plays a key role in atherogenesis. Patients with glycogen storage disease type Ia (GSD Ia) do not develop premature atherosclerosis despite severe hyperlipidemia. We analyzed antioxidative defense and oxidative stress in plasma and serum of patients with GSD Ia (n = 17) compared to patients with type I diabetes mellitus (DMI, n = 17), familial hypercholesterolemia (FH, n = 18), and healthy controls (n = 20). We measured the total radical-trapping antioxidant parameter (TRAP), single antioxidants (sulfhydryl groups, uric acid, vitamin C, alpha-tocopherol, coenzyme Q10), malondialdehyde, oxidized low density lipoprotein (LDL) antibodies, lipid profile [cholesterol, triglyceride, lipoprotein (a)], homocysteine, and hemoglobin (Hb)A(1C). TRAP levels were elevated in the GSD Ia group (p <.01) and correlated with elevated uric acid levels (r = 0.72, p =.001). None of the other plasma antioxidants correlated with TRAP levels. DMI patients showed decreased sulfhydryl groups (p <.01) and a reduced ubiquinol-10 fraction (p <.01). Malondialdehyde (p <.001) and oxidized LDL autoantibodies (p <.05) were increased in the diabetic group. In FH patients, parameters of oxidative stress and TRAP did not differ from controls. We conclude that in GSD Ia an increased antioxidative defense in plasma may protect against lipid peroxidation and thus against premature atherosclerosis. Furthermore, we demonstrated that in DMI increased oxidative mechanisms are already present in childhood.
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PMID:Plasma antioxidants in pediatric patients with glycogen storage disease, diabetes mellitus, and hypercholesterolemia. 1208 88

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