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)

Chromium (Cr) improves the glucose/insulin system in subjects with hypoglycemia, hyperglycemia, diabetes and hyperlipemia with no detectable effects on control subjects. Chromium improves insulin binding, insulin receptor number, insulin internalization, beta cell sensitivity and insulin receptor enzymes with overall increases in insulin sensitivity. There have been several studies involving Cr supplementation of subjects with NIDDM and/or lipemia and most have reported beneficial effects of Cr on the glucose/insulin system. In a recent study, Chinese subjects with NIDDM were divided into three groups of 60 subjects and supplemented with placebo, 100 or 500 micrograms of Cr as chromium picolinate 2 times per day for 4 months. Improvements in the glucose/insulin system were highly significant in the subjects receiving 500 micrograms twice per day with less or no significant improvements in the subjects receiving 100 micrograms twice per day after 2 and 4 months. In summary, Cr is involved in the control of the glucose/insulin system and the amount, and likely form of chromium, are critical when evaluating the role of chromium in this system.
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PMID:Nutritional factors influencing the glucose/insulin system: chromium. 932 87

Ketogenic diet therapy has been found to be an effective means of treating afebrile seizures that are refractory to antiepileptic medication alone. Controversies exist regarding its use. Potential harmful side effects include Staphylococcus aureus infections, retarded growth, hypoglycemia, hyperlipidemia, urolithiasis, and optic neuropathy. Pediatric nurses with knowledge about ketogenic diet therapy and current research regarding its use, will be better able to determine the appropriateness of this form of therapy for children with seizures that cannot be controlled by medication alone.
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PMID:Use of the ketogenic diet in treating children with seizures. 935 82

Nutrition management is an integral part of overall diabetic treatment that includes insulin, physical activity, emotional support and guidance. The aim of the present study was to evaluate a dietary approach in line with the recommended dietary allowances in terms of protein, total and saturated fat, carbohydrates as well as fibre and polyunsaturated fatty acid. A correct dietary approach may help to prevent and to reduce to a minimum any risk of hyperglycaemia, hypoglycaemia and important long-term complications such as obesity, hyperlipidaemia and hypertension, and at the same time normal growth development.
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PMID:The role of nutrition in prevention of complications in insulin-dependent diabetes mellitus. 1019 53

Glycogen storage disease type 1 (GSD-1), also known as von Gierke disease, is caused by a deficiency in the activity of the enzyme glucose-6-phosphatase (G6Pase). It is an autosomal recessive disorder characterized by hypoglycemia, hepatomegaly, kidney enlargement, growth retardation, lactic acidemia, hyperlipidemia and hyperuricemia. The disease presents with both clinical and biochemical heterogeneity consistent with the existence of two major subgroups, GSD-1a and GSD-1b, which have been confirmed at the molecular genetic level. GSD-1a, the most prevalent form, is caused by mutations in the G6Pase gene that abolish or greatly reduce enzymatic activity. The gene maps to chromosome 17q21 and encodes a microsomal transmembrane protein. Animal models of GSD-1a exist and are being exploited to delineate the disease more precisely. It has been proposed that GSD-1b is caused by a defect in the microsomal glucose-6-phosphate transporter. The gene responsible for GSD-1b has been mapped to chromosome 11q23 and a cDNA encoding a microsomal transmembrane protein has been identified. The function of this putative GSD-1b protein remains to be determined. These recent developments, along with newly characterized animal models of GSD-1a, are increasing our understanding of the interrelationship between the components of the G6Pase complex and type 1 glycogen storage diseases.
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PMID:Molecular Genetics of Type 1 Glycogen Storage Diseases. 1032 3

Glycogen storage disease type 1a (GSD-1a), characterized by hypoglycemia, liver and kidney enlargement, growth retardation, hyperlipidemia, and hyperuricemia, is caused by a deficiency in glucose-6-phosphatase (G6Pase), a key enzyme in glucose homeostasis. To evaluate the feasibility of gene replacement therapy for GSD-1a, we have infused adenoviral vector containing the murine G6Pase gene (Ad-mG6Pase) into G6Pase-deficient (G6Pase(-/-)) mice that manifest symptoms characteristic of human GSD-1a. Whereas <15% of G6Pase(-/-) mice under glucose therapy survived weaning, a 100% survival rate was achieved when G6Pase(-/-) mice were infused with Ad-mG6Pase, 90% of which lived to 3 months of age. Hepatic G6Pase activity in Ad-mG6Pase-infused mice was restored to 19% of that in G6Pase(+/+) mice at 7-14 days post-infusion; the activity persisted for at least 70 days. Ad-mG6Pase infusion also greatly improved growth of G6Pase(-/-) mice and normalized plasma glucose, cholesterol, triglyceride, and uric acid profiles. Furthermore, liver and kidney enlargement was less pronounced with near-normal levels of glycogen depositions in both organs. Our data demonstrate that a single administration of a recombinant adenoviral vector can alleviate the pathological manifestations of GSD-1a in mice, suggesting that this disorder in humans can potentially be corrected by gene therapy.
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PMID:Correction of glycogen storage disease type 1a in a mouse model by gene therapy. 1062 14

Decision levels of diabetes mellitus and hyperlipidemia in elderly subjects as well as younger subjects should be determined to prevent complications of these diseases such as microvascular and macrovascular diseases. Therefore, prospective follow-up study is necessary to decide the decision levels. In the case of diabetes mellitus, there are some useful studies such as KUMAMOTO STUDY show that strict glycemic control can prevent microvascular diseases, but there are few studies in elderly subjects. However, hypoglycemia causes macrovascular events, and chronic hypoglycemia leads to dementia and apathy. It is generally accepted that the glycemic control level can be milder than that in younger subjects. We suggest that the following decision levels are reasonable for elderly diabetic subjects, 1. FPG > 140-160 mg/dl, 2. PG(2 h) > 200-250 mg/dl, 3. HbA1c > 7-8%. Decision level of hyperlipidemia in elderly subjects should also be determined to prevent cardiovascular disease. It is demonstrated that anti-hyperlipidemic treatment can prevent CHD even in elderly subjects by many prospective studies. Japan Atherosclerosis Society recommend that the decision levels of hyperlipidemia in elderly subjects can be the same as younger subjects. The decision levels indicating diet therapy and medication for risk factor free subjects(category A) are LDL-C > or = 140 and 160 mg/dl, respectively. Those for subjects without CHD but have some risk factors(category B) are LDL-C > or = 120 and 140 mg/dl, respectively. Those for subjects with CHD(category C) are LDL-C > or = 100 and 120 mg/dl, respectively.
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PMID:[Decision levels of diabetes mellitus and hyperlipidemia in elderly Japanese subjects]. 1080 29

This study was designed to determine changes in myocardial contractile function and fuel selection during moderate coronary hypoperfusion in the presence of elevated plasma free fatty acid (FFA) at normal and reduced blood glucose concentrations. Coronary perfusion pressure (CPP) was sequentially lowered from 100 to 60, 50, and 40 mmHg in the left anterior descending coronary artery (LAD) of anesthetized, open-chest dogs. Regional glucose uptake (GU), fatty acid uptake (FAU), percentage segment shortening (%SS), and oxygen consumption (MV O(2)) were determined with normal arterial plasma FFA concentrations (Group 1) or with elevated FFA concentrations (Groups 2 and 3). In Group 3, glucose in the coronary perfusate blood was reduced from 3.53+/-0.36 to 0.15+/-0.03 m M by hemodialysis. In Group 1, FAU fell by 85% as CPP was lowered to 60 mmHg and remained depressed as CPP was reduced further; GU did not fall significantly. Hyperlipidemia in Group 2 did not alter GU at any CPP, but maintained FAU at baseline levels until CPP was lowered to 40 mmHg. At 40 mmHg CPP, myocardial function and metabolic variables were similar in Groups 1 and 2. In Group 3 at 40 mmHg, FAU increased four-fold and MV O(2)doubled v Groups 1 and 2, and GU fell to zero. Despite these metabolic changes, %SS in Group 3 was unchanged relative to Group 2. Addition of glucose to the dialysate prevented the effects of dialysis on FAU, GU, and MV O(2). Thus, preferential glucose oxidation sustains myocardial oxygen utilization efficiency [(heart rate x %SS x maximum left ventricular pressure)/MV O(2)] during hypoperfusion. Blocking preferential glucose oxidation by combined hyperlipidemia and hypoglycemia lowers oxygen utilization efficiency, but does not compromise myocardial contractile function.
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PMID:Hyperlipidemia with hypoglycemia reduces myocardial oxygen utilization efficiency but not contractile function during coronary hypoperfusion. 1090 Jan 79

Vanadium, a trace element in human cells and regarded as an essential nutrient, plays an active role in all tissues. It is known that peroxovanadate-nicotinic acid (POV), a complex compound of vanadium, can decrease hyperglycemia; however, its biochemical mechanism remains unclear. The object of the present study is to explore the hypoglycemia mechanism of POV at gene molecular levels. Rats rendered diabetic with streptozotocin were treated with POV. Total RNA was isolated from rat liver, and phenylalanine hydroxylase (PAH) mRNA abundance was determined by reverse transcriptase-polymerase chain reaction. PAH activity, blood glucose, and lipid levels were measured. Significantly increased hepatic PAH activity and corresponding mRNA with concomitant hyperglycemia and hyperlipemia were found in diabetic rats. These levels returned to normal after POV treatment and accompanied by negative glucosuria, normoglycemia, and normolipemia. The results from the current study indicates one of the mechanisms of POV action is to inhibit PAH gene expression and PAH activity, thus decreasing gluconeogenesis and hyperglycemia. At the same time, POV is able to promote diabetic recovery by lowering hyperlipemia.
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PMID:Effect of peroxovanadate compound on phenylalanine hydroxylase gene expression. 1105 10

Carnitine palmitoyltransferase type I (CPT I) is unique among long-chain fatty acid oxidation enzymes in that there are two tissue-specific isoforms, 'hepatic' and 'muscle', which are encoded by two separate genes. The 'hepatic' isoform is expressed in liver, kidney and fibroblasts and at low levels in the heart, while the other isoform occurs in skeletal muscle and is the predominant form in heart. Reported patients with CPT I deficiency lack activity of the hepatic isoform and present before 30 months of age with hypoketotic hypoglycaemia, hepatomegaly with raised transaminases, seizures and coma. We discuss four new cases in three families showing, variously, renal tubular acidosis, transient hyperlipidaemia and, paradoxically, myopathy with elevated creatinine kinase or cardiac involvement in the neonatal period as additional features that deserve wider recognition.
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PMID:Features of carnitine palmitoyltransferase type I deficiency. 1128 80

Mutations in the glucose-6-phosphatase (G6Pase) gene are responsible for glycogen storage disease type Ia (GSDIa). This disease is characterized by growth retardation, hepatomegaly, hypoglycemia, hyperlipidemia, and lactic acidosis. In this study, we report mutations in the G6Pase gene in 8 of 25 Brazilian patients with clinical symptoms of GSDIa. Five previously described mutations (R83C, Q347X, V338F, D38V, and G68R) were detected. The two most common mutations identified were R83C and Q347X, accounting for 8 of 14 (57.14%) mutant alleles. A 1,176 single-nucleotide polymorphism and two intronic mutations (IVS3-58T>A and IVS4+10G>A) were also analyzed. We used the minigene strategy in order to verify the effect of these intronic mutations on the splicing mechanism. This study emphasizes that molecular genetic analysis is a reliable and convenient alternative to the assay of enzyme activity in a fresh liver biopsy specimen for diagnosing GSDIa.
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PMID:Glycogen storage disease type Ia: molecular study in Brazilian patients. 1131 May 82


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