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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and biochemical features of eleven patients with Type V hyperlipoproteinaemia have been reviewed. All patients were male, and there was a high incidence in the group of obesity, vascular disease, acute abdominal pain, gout, diabetes mellitus and alcoholism. Plasma cholesterol concentrations ranged from 212 to 1512 mg/100ml and triglycerides from 708 to 7670 mg/100 ml. Lipaemia was associated with significant hyponatraemia, and also interfered with the determination of plasma glucose and serum amylase. Chylomicronaemia and hyperprebetalipoproteinaemia were accompanied by reduction in the pools of beta and alpha lipoproteins. All lipoprotein classes were relatively depleted of cholesterol compared to triglyceride. There was a variable pattern of treatment response. In some patients alcohol withdrawal produced a rapid improvement in plasma lipids. In diabetes mellitus there were two types of response: a rapid one in chronic insulin deficiency, and secondly, a more gradual one in mild diabetes associated with hyperinsulinaemia. In other patients there was a rapid response to carbohydrate-calorie restriction but the respective contributions of each of the steps remained unclear.
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PMID:Type V hyperlipoproteinaemia re-visted: findings in a sydney population. 16 79

The nature of Type V hyperlipoproteinemia including mode of presentation, prominent clinical and biochemical features, and genetics, was examined in 29 adults presenting with the Type V lipoprotein phenotype. Initially 23 of the 29 patients had various metabolic stimuli (diabetes out of control, estrogenic agents, pancreatitis, ethanolism) superposed on their acute hypertriglyceridemia. After metabolic stabilization, 17 of the 29 subjects were shown to have familial hypertriglyceridemia. In the 17 kindreds with familial hypertriglyceridemia, the lack of a specific, distinctive genetic marker for the Type V genotype and for the Type IV genotype restricts the conclusion that the pattern of inheritance was consistent with an autosomal dominant trait.
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PMID:Familial and acquired type V hyperlipoproteinemia. 107 94

Studies of adipocyte metabolism were performed in twelve male subjects with normal plasma lipids and eleven male patients with Type IV or Type V hyperlipoproteinemia. Patients with obesity or diabetes mellitus were excluded from the study. Although all patients had normal glucose tolerance tests, the blood glucose levels during these tests were higher in the hyperlipoproteinemic patients than in the normal control subjects and the plasma insulin responses were even more strikingly elevated in the hyperlipemic group. Adipocytes isolated from hypertriglyceridemic subjects were larger than those obtained from normal individuals and exhibited increased activities of both Type I and Type II hexokinase and increased rates of glucose oxidation and lipogenesis from glucose. Cell size, hexokinase isoenzyme activities and rates of lipogenesis from glucose were all strongly correlated with each other, but none of these measurements were correlated with glucose oxidation. It is not known how the adipocyte abnormalities are related to the lipid transport disorder.
Diabetes 1975 Feb
PMID:Hyperinsulinemia and enlarged adipocytes in patients with endogenous hyperlipoproteinemia without obesity or diabetes mellitus. 112 8

Type V hyperlipoproteinemia is characterized by elevations of chylomicron (CM) and very low density lipoprotein (VLDL) triglycerides. The development of this lipid disorder involves a multitude of metabolic derangements including deficient clearance of triglycerides and/or their increased output aggravated by obesity, diabetes, alcohol intake, or use of some hormones. Some studies have suggested that the apolipoprotein E4 phenotype is involved in this dyslipoproteinemia but this concept is still a matter of controversy. Therefore, we determined the apoE phenotype in 21 patients with severe hypertriglyceridemia classified as type V. Their apoE4 gene frequency was 0.595 which is 2.6-fold higher (P less than 0.001) than that in the Finnish population. Correspondingly, their apoE3 gene frequency was lower than that in the normal population. No differences were noted in plasma lipoproteins of the apoE4 phenotypes and the other type V subjects. The apolipoprotein C-II and C-III distribution was similar to that in normolipidemic subjects. The results suggest that apoE4 may be involved in the development of type V hyperlipoproteinemia.
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PMID:Role of apolipoproteins E and C in type V hyperlipoproteinemia. 337 42

Type V hyperlipoproteinaemia complicated a pregnancy in a 38 year old Samoan multigravida with previous noninsulin dependent diabetes. The hypertriglyceridaemia was associated with severe insulin resistance, nonacidotic ketosis and poor control of the diabetes. Continuous subcutaneous insulin infusion resulted in excellent diabetic control and plasma triglyceride levels fell to normal without specific dietary fat restriction. The pregnancy resulted in the live birth of a normal healthy infant at 38 weeks' gestation.
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PMID:Pregnancy complicated by non-insulin dependent diabetes mellitus and type V hyperlipoproteinaemia: case report. 385 32

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.
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PMID:The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients. 711 4

Type V hyperlipoproteinemia is an unusual entity in children. Only 6 cases have been described so far to our knowledge. Authors present a 9 year old male that came for diagnosis of a hepatosplenomegaly. There was no evidence of abdominal pain, xanthomas or pancreatitis. Secondary disorders such as uncontrolled insulinopenic diabetes mellitus, glycogen storage disease, administration of estrogen compounds, nephrotic syndrome or uremia, and dysglobulinemias were excluded. His father presented the same lipoprotein pattern suggesting a dominant mode of inheritance. The administration of heparin showed a good response of serum proteinlipase.
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PMID:[Primary hyperlipoproteinemia in childhood (author's transl)]. 728 88

Familial lipodystrophy is a genetically heterogeneous set of disorders characterized by a total or partial absence of subcutaneous fat, diabetes mellitus or impaired glucose tolerance, hyperlipidemia, and hypermetabolism [Senior and Gellis, 1964]. One subtype, familial partial lipodystrophy Dunnigan (FPLD), is a rare autosomal dominant trait that results in an gradual loss of subcutaneous fat in the lower trunk and limbs, Type V hyperlipoproteinemia, hypertriglyceridemia, and insulin-resistant diabetes. Previous reports of this condition have been limited to case reports or very small families. Recently, Peters et al. reported on linkage of five families of Western European descent to a 5.3 cM region on chromosome 1q21-22 between the flanking markers D1S305 and D1S1600 [Peters et al., 1998: Nat Genet 18:292-295]. We performed linkage and haplotype analysis using highly polymorphic, microsatellite markers on a large, multigeneration Caucasian kindred of German ancestry. The maximum two-point lod score achieved was 4.96 at theta(max) = 0 for marker D1S2721. Multipoint analysis gave an overall maximum lod score of 6.27 near marker D1S2721. The results of the haplotype analysis support the minimal candidate region as reported by Peters et al.
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PMID:Confirmation of linkage of hereditary partial lipodystrophy to chromosome 1q21-22. 993 82