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

The faecal output of bile acids and endogenous neutral steroids was increased in three hypertriglyceridaemic patients. One patient had familail type IIb, one had type IV and the third had type V hyperlipoproteinaemia. The hyperlipidaemia in the type IV and type V patients was associated with diabetes and a high alcohol intake. The plasma cholesterol and triglyceride concentrations and the faecal output of bile acids decreased significantly when the type IIb patient was given D-thyroxine plus propranolol, and when the type IV and type V patients were treated by withdrawal of alcohol, a low=carbohydrate diet and insulin or glibenclamide. The findings are discussed in relation to the possibility that hypertriglyceridaemia and increased bile acid synthesis in these patients have a common metabolic origin.
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PMID:Cholesterol metabolism in hypertriglyceridaemia and the effects of treatment. 17 61

A woman, aged 46 years, with a hyperlipoproteinemia phenotype V, an unusual type of xanthomatosis, as well as lipemia retinalis, diabetes mellitus, and nephropathia, is discussed. The withdrawal of 64 IU insulin and the institution of a hypocaloric diabetes diet resulted in the disappearance of the skin lesions and a regression of the eye lesion. During this treatment the total lipid-level became almost normal (6,965 mg% before treatment and 947 mg% after 10 weeks). The chylomicrons disappeared but the VLDL content remained relatively and absolutely elevated, as in type IV hyperlipoproteinemia.
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PMID:A case of xanthomatosis and hyperlipoproteinemia type V propably induced by overdosage of insulin. 17 87

The metabolism of lipoprotein-apoprotein was examined in four subjects with normal lipid metabolism and in one subject with type II hyperlipemia by means of isotopic tracer methodology. Studies were performed after intravenous injection of a radioactive amino acid precursor for apoprotein synthesis (75Se-selenomethionine), in both the basal state and following the acute injection of intravenous heparin. Computer technics were used to evaluate a series of multicompartmental models, and a general model is proposed that yields optimum fitting of experimental data for serum free amino acid precursor, very-low-density lipoprotein-apoprotein (VLD-apoprotein), and low-density lipoprotein-apoprotein (LDL-apoprotein) in man. The analysis demonstrates that approximately half of the transport of 75Se-apoVLDL from the plasma VLDL pool is converted to 75Se-apoLDL. The acute injection of heparin in two normal subjects results in a two-and-a-half-fold increase in this rate of conversion of 75Se-apoVLDL to 75Se-apoLDL. 75Se-apoLDL is metabolized by rapid transport into a recycling extravascular pool and by irreversible catabolism. The fractional rate of recycling is large relative to the fractional rate of catabolism of apoLDL (3.7:1.0), suggesting extravascular recycling as a potential site of regulation of the plasma concentration of apoLDL. In a patient with type II hyperlipemia, the extravascular recycling pathway is reduced and is not corrected with D-thyroxine therapy. However, this therapy did reduce conversion of apoVLDL to apoLDL in this type II patient. The kinetic data support the validity of the compartmental model in simulating both normal and pathologic apoprotein metabolism and that perturbation of physiology seen with heparin injection and D-thyroxine therapy. These data support a quantitative role of apoVLDL as a precursor of apoLDL and identify an important recycling pathway of apoLDL metabolism in addition to that of catabolism.
Diabetes 1976 Aug
PMID:Incorporation of 75Se-selenomethionine into human apoproteins. III. Kinetic behavior of isotopically labeled plasma apoprotein in man. 18 7

There are several causes for hyperlipemia in the diabetic: (a) an increase in hepatic synthesis of prebetalipoproteins, and (b) reduced elimination of prebetalipoproteins and chylomicrons from the bloodstream, due to diminished activity of lipoprotein lipase in insulin deficiency. The role of heredity has been put in doubt by the observation that diabetes and hypertriglyceridemia are not transmitted by the same genetic factor. The shortterm and longterm implications of diabetic hyperlipemia are discussed, together with the treatment.
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PMID:[Hyperlipemia and diabetes]. 18 65

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.
Diabetes 1977 Jan
PMID:Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism. 18 16

There is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
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PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

The authors present the results of prospective study of the blood serum lipids (total cholesterol, triglycerides, lipoproteid fractions) in 132 patients with diabetes mellitus aged from 35 to 60 years and in 47 healthy persons of the same age (control group). The majority of the patients examined (60.6%) showed hyperlipidemia; types II and IV were most frequent. An increase in the content of the probeta-lipoproteid fraction and hypertriglyceridemia were mostly encountered in patients with macroangiopathies, particularly in the presence of adiposity. There was revealed no significant relationship between the frequency of hyperlipidemia and the severity of diabetes mellitus. However, the most distinct lipid disturbances were found in the patients with the disease of moderate severity. This was apparently connected with the prevalence in this group of persons with an excessive weight. As revealed, the incidence of hyperlipidemia rose on account of increased level of both total cholesterol and of triglycerides (with a tendency to their greater content in women).
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PMID:[Disorders of lipid content of blood in diabetes mellitus]. 20 21

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

Type V hyperlipemia is not very common. The series of 54 cases descrubed here is the largest reported to date. Our observations were recorded when lipidograms showed the presence of chylomicrons and a large pre-beta-lipoprotein spot in the serum of fasting subjects. Type V hyperlipemia was often combined with other metabolic syndromes such as diabetes, hyperuricemia or gout, or obesity. Chronic alcoholism was also noted in half our subjects, in whom hyperlipemia quickly regressed after alcohol consumption ceased. Ischemic arterial complications, chiefly coronary, were found in one third of our cases, and the vascular risks accompanying this type of hyperlipemia rose considerably in patients with high blood pressure. Various type of treatment were administered, but all subjects were put on a special diet, comprising either the elimination of alcoholic drinks only, or, in addition to this, reduced carbohydrate or calorie intake. As a rule, these measures resulted in a distinct regression of lipid anomalies. Clofibrate or derivatives proved effective in cases where hyperlipemia failed to respond to dietary measures.
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PMID:[Type V hyperlipemia. 54 cases (author's transl)]. 22 80

A case of diabetic lipemia is reported in a 27 year-old man admitted for acute pancreatitis. Initial investigations revealed gross hyperlipoproteinemia and ketoacidosis. Hyperlipoproteinemia was progressively corrected up to normalization in four weeks under insulin-therapy; the metabolic control of diabetes was obtained in parellel. This feature is caracteristic of "diabetic lipemia". The following sequence could be suggested: onset of diabetes, occurence of diabetic lipemia and then acute pancreatitis.
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PMID:[Acute pancreatitis during "diabetic lipemia": unusual disclosure of insulin-dependent diabetes (author's transl)]. 22 21


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