Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splanchnic metabolism was studied to quantify changes underlying the fatty liver, hyperlipemia, and hypoglycemia produced by ethanol. Four subjects fasted for 15 h were compared with five subjects fasted for 69 h under basal conditions and during continuous intravenous infusion of sufficient ethanol to give a concentration of 3-5 mM in arterial blood plasma. Splanchnic storage of fatty acids was estimated from the difference between uptake of FFA and secretion of derived products. Basal values for splanchnic uptake of FFA were twofold higher after the 69-h fast while splanchnic storage of fatty acids and production of ketone bodies increased threefold. Values for basal secreation into the blood of triglycerides derived from FFA were similar in the two groups. In both nutritional states, the fraction of FFA taken up in the splanchnic region oxidized to ketone bodies and to CO2 fell when ethanol was given because of preferential oxidation of ethanol to acetate, and the fraction esterified rose. However, systemic transport and splanchnic uptake of FFA fell with ethanol in subjects fasted 15 h, so that neither storage of triglycerides in splanchnic tissues nor secretion into the blood increased. In subjects fasted 69 h, ethanol increased transport of FFA and splanchnic storage of fat. In all but one subject it also increased secretion of triglycerides into the blood. The concentration of glucose in blood fell during ethanol infusion in all five subjects undergoing the 69-h fast. Mean splanchnic glucose production was maintained at about one-half of the pre-ethanol value, despite virtual cessation of splanchnic uptake of lactate and of those amino acids that are metabolized via malate. Quantitative estimates of extrasplanchnic metabolism suggest that enhanced formation of alpha-glycerophosphate from glucose, in addition to impaired hepatic gluconeogenesis, may contribute to ethanol-induced hypoglycemia in man.
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PMID:Effects of a 3-day fast and of ethanol on splanchnic metabolism of FFA, amino acids, and carbohydrates in healthy young men. 17 79

Three children with defective gluconeogenesis and hypoglycemia were treated with frequent daytime feeding and continuous intragastric infusion of glucose at night. By this technique, the blood glucose level was maintained at or slightly above the physiological range. Secondary lacticacidemia, hyperlipidemia, hyperuricacidemia, and coagulation defects all improved. Weight and height velocity increased dramatically. Strength and sense of well-being improved. Nocturnal intragastric infusion of glucose is now the management of choice for children with defective gluconeogenesis and hypoglycemia.
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PMID:Nocturnal intragastric infusion of glucose in management of defective gluconeogenesis with hypoglycemia. 27 48

600 mg of bezafibrate daily were administered to 13 well controlled diabetics with hyperlipidaemia for 12 weeks. Placebo was given before and after the treatment period. Compared with pretreatment placebo, bezafibrate reduced triglycerides (between 37 and 47%) and cholesterol (between 12 and 19%) significantly. Blood glucose levels during treatment were significantly lower at 8 and 12 weeks compared with post-treatment placebo values. Urinary glucose excretion did not change. Hypoglycaemia was not observed. No change in antidiabetic medication was necessary. Bezafibrate was well tolerated. It lowered blood lipids effectively in diabetics with hyperlipidaemia. No additional precautions have to be taken to control carbohydrate metabolism during bezafibrate treatment.
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PMID:[Lipid-lowering effect of bezafibrate in patients with diabetes mellitus and hyperlipidaemia (author's transl)]. 66 70

Two main classes of oral hypoglycaemic drugs, the sulphonylureas and the biguanides, are currently used in the therapy of type II, non-insulin-dependent diabetes mellitus (NIDDM). The basic pharmacokinetic properties of these agents are discussed with a view to efficient and safe treatment. Both first- and second-generation sulphonylureas are rapidly absorbed from the gastrointestinal tract. In the plasma compartment, these drugs are strongly bound to serum proteins. All sulphonylureas are metabolised in the liver, and the metabolites and the parent drugs are eliminated mainly in the urine, but also (second-generation derivatives) in the faces. Rapid- and short-acting sulphonylureas may improve early insulin release and promote better postprandial glucose control. Long-acting derivatives may ensure better control of overnight glycaemia. The elderly are at risk of developing severe sulphonylurea-induced hypoglycaemia, and in this population the agent chosen should have a short or intermediate duration of action and no active metabolites. Caution is needed when prescribing any sulphonylurea in patients receiving drugs known to affect sulphonylurea action, and in those with impaired liver and/or kidney function. The bioavailability of the biguanides ranges from 40 to 60%. Binding to plasma proteins is absent or very low. Metformin and buformin are not metabolised and are excreted in the urine; phenformin undergoes hepatic hydroxylation and is excreted in both urine and faeces. Metformin is the only agent of this class currently recommended for clinical use. The main indications of metformin treatment are NIDDM associated with obesity and/or hyperlipidaemia, and in combination with sulphonylurea both as primary treatment and when secondary failure occurs with sulphonylurea alone. Lactic acidosis may develop in patients receiving therapy with biguanides, especially in the presence of a preexisting contraindication to their use.
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PMID:Pharmacokinetic optimisation of oral hypoglycaemic therapy. 176 Sep 2

Renal disease is a frequent and serious complication of type I glycogen storage disease. A type I glycogen storage disease patient with focal segmental glomerulosclerosis and progressive renal insufficiency underwent a renal allograft transplantation. Despite the same cornstarch therapy, the post-transplantation course was complicated by worsening of the metabolic control manifested by exacerbated lactic acidaemia and hyperlipidaemia. This lactic acidaemia was remarkable for its association with hyperglycaemia. Hyperglycaemia accompanied by lactic acidaemia is strikingly unusual in type I glycogen storage disease, since this is a disease characterized by hypoglycaemia and an inverse relationship between blood glucose concentration and lactate levels. Both fasting insulin and C-peptide levels in the patient were greater than similar age-matched type I glycogen storage disease controls, indicating hyperinsulinaemia. The most likely mechanism responsible for the combined hyperglycaemia and lactic acidaemia was insulin resistance due to glucocorticoid treatment, instituted for immunosuppression. The hyperglycaemia associated with the lactic acidaemia was transient and resolved with steroid tapering. The exacerbated hyperlipidaemia, however, persisted after renal transplantation. Type I glycogen storage disease patients may be prone to glucocorticoid-induced insulin resistance, since the cellular metabolism in these patients may already be compromised with ineffective insulin action and/or reduced insulin output.
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PMID:Hyperglycaemia associated with lactic acidaemia in a renal allograft recipient with type I glycogen storage disease. 186 63

The criteria for the diagnosis of diabetes are the same in all age groups. The main reason for a deterioration of glucose tolerance with age is insulin resistance, primarily concerning glucose uptake of skeletal muscle. The decision of if and how diabetes is treated in old people is a highly individual one depending on the patient's general condition and life circumstances. Acute symptoms are poorly characteristic and can be mistaken as complaints of old age, thus they play the most important role in deciding therapy. Diet is the most important role in deciding therapy. Diet is the most important therapy and the only therapeutic aspect without side-effects. The patients habits must be known before prescribing a practical diet. Besides general principles of a diabetic diet, hyperlipidemia and hypertension, and also deficiencies in nutrients must be taken into account. By reducing insulin resistance, exercise training can excellently support dietary therapy. Additional drug therapy should certainly be started if acute symptoms persist with proper diet, or if fasting glucose concentrations in plasma exceed 200 mg/dl. Acarbose, metformin, sulfonylureas, and insulin are the drugs available, of which mechanisms of action, applications, and side-effects are described. In the order given the efficacy of these drugs as well as the risk of dangerous side-effects increases. If sulfonylureas or insulins are applied for treatment the risks of hypoglycemia must be explained to the patient and his family, and must be prevented by all means. Finally, the importance of treating the diseases accompanying and following diabetes is stressed.
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PMID:[Current principles of therapy of diabetes mellitus in old age]. 195 85

The renal disease in an adult woman with Type 1 glycogen storage disease (GSD) is reported. Since she was 15 years old, several episodes of gouty arthritis had developed. At the age of 18, proteinuria was pointed out. Hepatomegaly, renomegaly out of proportion to the impairment of renal function, hyperuricemia, hyperlipidemia, fasting hypoglycemia and lactic acidemia were observed. The diagnosis of GSD was established on the basis of a glucose tolerance test, glucagon test and liver biopsy. The findings of renal biopsies performed at the ages of 24 and 27 years old suggested that glomerular damage might have preceded the tubulo-interstitial lesion.
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PMID:Renal disease in an adult with type 1 glycogen storage disease. 203 36

A 31-year-old male patient with type Ia glycogen storage disease was admitted to our department complaining of general fatigue and right hypochondriac pain. He exhibited massive hepatomegaly with systemic hypoglycemia, lactic acidosis, hyperuricemia, hyperpyruvatemia and hyperlipemia. The failure of blood glucose levels to increase after a glucagon loading test, and a reduced lactate level on glucose tolerance test were also observed. Various imaging techniques suggested hepatic adenoma with hemorrhage in the tumor, which was confirmed histologically. There was a complete absence of glucose 6-phosphatase activity, as determined by an enzyme assay on resected liver specimens, which proved the case to be type Ia glycogen storage disease. We also reviewed all previously reported cases of hepatic tumor and glycogen storage diseases. We conclude that, since hepatic adenoma is not rare in this disease, and is complicated by hemorrhage, rupture and malignancy, careful follow-ups are necessary.
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PMID:A case of type Ia glycogen storage disease complicated by hepatic adenoma. 217 Feb 59

Type II diabetes mellitus may affect as many as 20% of the elderly US population. In the absence of data to support the need to maintain a specific level of glucose beyond that necessary to relieve symptoms, choice of therapy is problematic. Clearly, supervised dietary therapy for the obese type II diabetic patient represents a safe and cost-effective treatment. For those patients who fail dietary therapy because they fail to lose weight or regain lost weight, or because blood glucose levels remain high despite weight loss, further therapy must be individualized. The only rational criteria for drug treatment supportable by currently available data are (1) persistent symptoms associated with hyperglycemia, (2) ketonuria in the unstressed state, and (3) certain cases of hyperlipidemia, especially with triglyceride levels greater than 1000 mg/dl. In these clinical settings, drug therapy is necessary to eliminate symptoms, prevent development of ketoacidosis, and reduce the risk of pancreatitis, respectively. Consideration of drug therapy should also be made in the case of very elevated blood glucose levels, even in the absence of symptoms, when dehydration and risk of severe hyperosmolarity exist. The issues regarding insulin versus sulfonylureas have not been examined specifically in the elderly population. Extrapolating from published studies that generally include patients older than 65 years leads to the following conclusions: Caution regarding adverse side effects of insulin (hypoglycemia, theoretic risk of hyperinsulinemia) and sulfonylureas (hypoglycemia, drug interactions, increased risk of cardiovascular death) must be balanced against the theoretic benefit of treatment in the absence of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in the elderly diabetic patient. 222 55

A rabbit model of catheter-related bacteremia was developed to study immunity to the capsular polysaccharide/adhesin (PS/A) of coagulase-negative staphylococci. Catheters colonized by coagulase-negative staphylococci were inserted into the right jugular vein and attached to a subcutaneous osmotic pump, and blood cultures were obtained over 14 days. Nonimmune rabbits were bacteremic for 6-8 days after infection, hypoglycemic, and hyperlipidemic and had strong immune responses to teichoic acid but not to PS/A. PS/A immunization, but not teichoic acid immunization, reduced the number of bacteremic days by approximately 60%, diminished the hypoglycemia and hyperlipidemia, and ablated the immune responses to teichoic acid. Passive infusion of PS/A-specific polyclonal and monoclonal antibodies using a separate, noninfected catheter-pump combination implanted in the left jugular protected against both bacteremia and hematogenous colonization of this contralateral catheter.
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PMID:Antibody to the capsular polysaccharide/adhesin protects rabbits against catheter-related bacteremia due to coagulase-negative staphylococci. 237 73


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