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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two episodes of acute aflatoxin poisoning in horses suggest that horses are susceptible to the toxic effects of this mycotoxin. Lesions associated with exposure to aflatoxin included encephalomalacia of cerebral hemispheres, fatty degeneration, necrosis, bile duct hyperplasia, fibrosis of the liver, fatty infiltration of the kidney, hemorrhagic enteritis, and myocardial degeneration. Hypoglycemia, hyperlipidemia, and depletion of lymphocytes accompanied these lesions. The diagnosis was based on gross and histopathologic observations, consistent with observations of other species poisoned with aflatoxin, and isolation of the toxin from feed and animal tissues. Removing contaminated feed prevented further morbidity or mortality.
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PMID:Aflatoxicosis in horses. 722 85

Chronic renal failure is characterized by abnormalities in glucose metabolism. In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. The glucose intolerance is not the result of reduced insulin secretion, or circulating insulin antagonists, and does not correlate with the coexisting metabolic acidosis. Glucose intolerance exists because the peripheral insulin-sensitive tissue (muscle, adipose tissue, liver) of the patients with chronic renal failure are insulin resistant. However there are two subgroups of uremic patients with regard to glucose tolerance: about half of uremic patients can augment their insulin secretion sufficiently to maintain normal glucose tolerance despite glucose intolerance. In the other half, insulin secretion following glucose loads is not different from normal values, so that glucose intolerance results. The cause of the peripheral insulin resistance remain unclear. Besides deranged renal function can result in the development of hypoglycemia. The most important predisposing mechanism to hypoglycemia is diminished glucose availability due to substrate limitation; the second important mechanism (alcohol, insulin, propranolol, etc.). Finally, in chronic renal failure persistent hyperinsulinemia can contribute hyperlipemia and to high incidence of cardiovascular disease.
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PMID:[Glucose metabolism and chronic renal insufficiency]. 801 26

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Diabetes mellitus with its resulting derangement of various metabolic fuels, carbohydrates, amino acids, lipids, and ketones has the potential to adversely affect the developing fetus. Therefore, strict glycemic control in pregnancy has become the standard of care in modern obstetrics. A considerable amount of research has been undertaken into the metabolic changes that occur during pregnancy in both women with insulin-dependent diabetes and gestational diabetes. This paper will review current research in normal and diabetic pregnancies both in the fasting and fed states as well as during episodes of hypoglycemia. In normal pregnancy insulin secretion increases throughout gestation whereas peripheral insulin sensitivity is decreased. Fasting levels of plasma glucose are reduced by approximately 10 per cent during the first trimester. Maternal amino acid levels are also reduced in normal pregnancy, although cholesterol and triglyceride levels are increased, most dramatically in the second trimester. As gestation advances, progressively increasing amounts of insulin antagonistic hormones are secreted by the placenta. This leads to gestational diabetes in 2 to 3 per cent of women who exhibit hyperglycemia despite an increased insulin response to oral glucose as well as an increased insulin/glucagon ratio. In insulin dependent diabetes mellitus, the insulin-deficient state results in fasting and postprandial hyperaminoacidemia, hyperlipidemia, and hyperglycemia. These metabolic changes and the resulting hyperglycemic milieu can lead to fetal macrosomia that will result in maternal and fetal morbidity. Therefore, normalization of these fuels with the use of intensive insulin regimens is the goal of therapy during pregnancy.
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PMID:Metabolic changes in diabetic and nondiabetic subjects during pregnancy. 813 54

Pharmacological suppression of lipolysis is being increasingly used in the treatment of diabetic hyperlipidaemia. Although theoretical hazard of such treatment is that recovery from hypoglycaemia might be impaired. Seven normal subjects were therefore studied on two occasions, following treatment with a single dose of either acipimox 250 mg or placebo. Hypoglycaemic recovery was unaffected, despite effective suppression of plasma non-esterified fatty acid levels with acipimox. The results suggest that under these conditions activation of lipolysis may not be essential to recovery from hypoglycaemia.
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PMID:Suppression of lipolysis in normal man does not inhibit recovery from insulin-induced hypoglycaemia. 844 73

The antihypertensive efficacy of single-drug therapy with nifedipine (N), prazosin (P), or acebutolol (A) and the influence of these agents on coronary risk factors including hypoglycemia, hyperuricemia, and hyperlipidemia, were studied in adolescents with hypertension. Ninety patients (73 girls and 17 boys) aged 14 to 18 years with idiopathic hypertension (IH) were randomized into three groups. Each group received N, P, or A as single-drug therapy for six months. Systolic and diastolic blood pressures fell in all three groups, from 152/90 mmHg to 127/70 mmHg* with N, from 150/90 mmHg to 121/70 mmHg* with P, and from 148/92 mmHg to 122/74 mmHg* mmHg with A. In 17% of cases, N failed to reduce blood pressures below the 90th centiles. Heart rate was not influenced by N or P but decreased from 84 to 75 bpm with A. Although none of the drugs modified serum uric acid levels, fractional uric acid secretion rose with P and A (from 4.1% to 6% with P; and from 4.4% to 6% with A). The lipid profile remained unchanged under N and P, whereas a decrease in serum LDL-cholesterol from 99.6 to 88.8% mg* was seen with A. Fasting serum glucose levels increased from 86.4 to 92.7 mg %* in the group given A. N, P, and A are suitable for single-drug therapy of IH in adolescents; the most appropriate drug should be selected on the basis of medical history.
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PMID:[Evaluation of the efficacy and tolerance of three antihypertensive agents used as single-drug therapy, nifedipine, prazosin and acebutolol in severe, idiopathic hypertension in adolescents]. 845 32

Insulin resistance resolved in 3 dogs with hypothyroidism and diabetes mellitus after treatment with sodium levothyroxine. A thorough diagnostic evaluation failed to identify any other cause of insulin resistance in these dogs. Hypothyroidism was diagnosed in each dog on the basis of clinical signs, physical findings, hyperlipidemia, and results of thyrotropin or thyrotropin-releasing hormone stimulation test. Hypoglycemia was documented in each dog within 2 weeks of starting sodium levothyroxine administration. The insulin dosage was decreased by 60 to 62% during the ensuing months and good glycemic control was obtained at these lower insulin dosages in all dogs. These findings would suggest hypothyroidism-induced insulin resistance in these dogs.
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PMID:Insulin resistance in three dogs with hypothyroidism and diabetes mellitus. 849 4

To investigate if growth hormone (GH) alters the effects of endotoxin in rats, endotoxin (5 mg kg-1 body weight) was injected into normal rats and into rats primed with GH for 3 days. Endotoxin had injurious effects on renal and liver function and induced hypoglycaemia and hyperlipidaemia as expected. GH-primed rats became extremely sick after endotoxin challenge and had more marked abnormalities of renal and liver function and much more pronounced hypoglycaemia and hyperlipidaemia than non-primed rats. It is concluded that growth hormone potentiates the in vivo biological activities of endotoxin in the rat. The results may also suggest that caution should be exerted when considering GH treatment in catabolic situations with endotoxaemia and that special attention should be paid to the prevention of infection during GH therapy in such situations.
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PMID:Growth hormone potentiates the in vivo biological activities of endotoxin in the rat. 890 56

We previously demonstrated that GH potentiates the biological activities of endotoxin in the rat. In the present study, we wanted to determine if the potentiating effects of GH on the biological activities of endotoxin could be reproduced by insulin-like growth factor I (IGF-I). Endotoxin (5 mg/kg BW) was injected in rats primed with or without GH or IGF-I for 3 days. As expected, endotoxin administration markedly increased circulating tumor necrosis factor (TNF) and interferon-gamma (IFN gamma) and induced organ injury, hypoglycemia, and hyperlipidemia. In GH-primed rats, endotoxin induced a further increase of serum IFN gamma (but not TNF); and five out of six of those rats died within 15 h after giving endotoxin. However, little difference between endotoxin-treated rats with and without IGF-I priming could be seen. Furthermore, IGF-I infusion altered blood glucose, urea, and circulating ICF-I levels more than GH infusion. Therefore, IGF-I does not enhance the biological activities of endotoxin in the rat, suggesting that the enhancement of endotoxin effects by GH is via an IGF-I-independent pathway. Priming rats by GH (but not by IGF-I) induced a further increased response of serum IFN gamma but not TNF to subsequent endotoxin challenge, suggesting that IFN gamma rather than TNF is likely to be involved in this process.
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PMID:Contrasting effects of growth hormone and insulin-like growth factor I on the biological activities of endotoxin in the rat. 897 16

Type 2 diabetes mellitus results from impaired insulin secretion and reduced peripheral insulin sensitivity. Treatment options include diet, oral antihyperglycemic agents, and insulin. Metformin, an oral biguanide, ameliorates hyperglycemia by improving peripheral sensitivity to insulin, and reducing gastrointestinal glucose absorption and hepatic glucose production. Unlike sulfonylureas, it does not stimulate insulin secretion, aggravate hyperinsulinemia, or cause hypoglycemia or weight gain (weight stabilizes or decreases). It also has beneficial effects on serum lipid profiles. In lean or overweight type 2 diabetic patients uncontrolled by diet, metformin monotherapy significantly improves glycemic control, compared with placebo, and to similar extents as sulfonylurea monotherapy. In secondary sulfonylurea failure, combination metformin-sulfonylurea treatment significantly improves glycemic control beyond that achieved with either agent along. Metformin-sulfonylurea also appears to be as effective as insulin or insulin plus sulfonylurea, suggesting that such combination therapy may obviate or substantially delay insulin therapy. Limited data suggest that metformin-insulin therapy may improve glycemic control, possibly reducing insulin requirements, in type 2 diabetic patients uncontrolled by insulin alone following secondary sulfonylurea failure. Gastrointestinal side effects are common, but usually tolerated. Lactic acidosis risk is minimal, provided that contraindications, particularly renal impairment, and prescribing guidelines are respected. Aside from elevated plasma metformin levels with cimetidine and synergistic hypoglycemia with sulfonylureas, few interactions occur. Thus, metformin is safe and effective both as monotherapy or in combination with other antihyperglycemic agents in type 2 diabetic patients requiring additional glycemic control and may be advantageous when weight control is desirable and/or hyperlipidemia exists.
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PMID:An overview of metformin in the treatment of type 2 diabetes mellitus. 920 6


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