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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been increasingly recognised in recent years that type 2 (non-insulin-dependent) diabetes is part of a cluster of cardiovascular risk factors known as the metabolic syndrome, but also endorsed with such names as the deadly quartet, syndrome X and the insulin resistance syndrome. Atherosclerosis is the most common complication of type 2 diabetes among Europeans, and coronary artery, cerebrovascular and peripheral vascular disease are 2 to 5 times more common in people with this condition than in those without diabetes. These observations indicate that the treatment of type 2 diabetes requires agents that do more than simply lower blood glucose levels, and a therapy with both antihyperglycaemic effects and beneficial effects on dyslipidaemia, hypertension, obesity, hyperinsulinaemia and insulin resistance is likely to be most useful. In this respect, metformin has an important and established role: this drug has been shown to lower blood glucose and triglyceride levels, and to assist with weight reduction and to reduce hyperinsulinaemia and insulin resistance. Studies in the Israeli sand rat, Psammomys obesus, have indicated hyperinsulinaemia/insulin resistance to be the initial and underlying metabolic disorder in obesity and type 2 diabetes. Thus, the well established effect of metformin in reducing insulin resistance makes this drug an excellent candidate for the prevention of progression of impaired glucose tolerance to type 2 diabetes, and for the reduction of mortality associated with cardiovascular disease.
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PMID:Clinical efficacy of metformin against insulin resistance parameters: sinking the iceberg. 1057 21

In 1988, Reaven used the term syndrome X to describe a relation between several disorders including hypertension, dyslipidemia, impaired glucose tolerance, obesity, and coronary heart disease. Despite a number of studies dealing with syndrome X, its genetic basis remains poorly understood. Regarding the complexity of this syndrome, it is important to use animal models developing the traits of the disease. Here we show a genetic dissection of syndrome X in the WOKW rat, an animal model of genetically determined syndrome X. We found a major quantitative trait locus (QTL) for glucose metabolism on chromosome 3 and further QTLs influencing obesity and body weight on chromosomes 1 and 5. Genetic determinants of dyslipidemia were mapped to chromosomes 4 and 17. In addition, suggestive linkage for serum insulin was found on chromosome 1 to the region previously shown to be associated with type-1 diabetes mellitus. This is the first study demonstrating independent genetic factors influencing traits of the syndrome X in the rat as well as a possible genetic relationships between syndrome X and diabetes mellitus. Moreover, regarding the close similarities between WOKW rat and human syndrome X, the study could help in a search of genetic factors involved in this complex metabolic disorder in human.
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PMID:Genetic dissection of the syndrome X in the rat. 1072 Apr 72

Although echocardiography is a useful diagnostic tool in hypertrophic cardiomyopathy (HCM), it is sometimes difficult to differentiate it from hypertensive heart disease (HHD): some patients with HCM show symmetrical hypertrophy, whereas patients with HHD sometimes show asymmetrical septal hypertrophy. We used a radioiodinated long-chain fatty acid tracer to visualize the altered myocardial fatty acid metabolism of HCM and HHD. Carnitine is the essential substance for the beta-oxidation of long-chain fatty acids. We recently reported that serum free carnitine levels in HCM were elevated and that they were significantly correlated with the severity of myocardial fatty acid metabolic disorder. Therefore, we investigated serum carnitine levels in patients with HCM and HHD, which can contribute to the differentiation of each other. We studied 56 patients with HCM and 20 patients with essential hypertension. Serum free carnitine levels were significantly higher in patients with HCM than those with HHD (HCM 52.5+/-9.5 nmol/mL, HHD 46.6+/-6.4 nmol/mL, P<0.01), but they showed no statistical difference between patients with HHD and normal subjects. Serum acylcarnitine levels were significantly lower in patients with HCM than those with HHD (HCM 10.1+/-4.0 nmol/mL, HHD 14.5+/-4.9 nmol/mL, P<0.0005), although they did not differ between patients with HHD and normal subjects. Scintigraphic analyses with a long-chain fatty acid analog revealed that myocardial tracer uptake was much reduced in patients with HCM compared with that in patients with HHD (quantitative analysis: HCM 2.11+/-0.12, HHD 2.22+/-0.17, P<0.05; semiquantitative analysis: HCM 13.6+/-6.3, HHD 2.0+/-1.5, P<0.0001). In conclusion, the differences in serum carnitine levels between HCM and HHD reflect altered myocardial fatty acid metabolic impairment, and the levels can help to distinguish these 2 diseases.
Hypertension 2000 Aug
PMID:Can serum carnitine levels distinguish hypertrophic cardiomyopathy from hypertensive hearts? 1094 80

Type 2 diabetes is a complex metabolic disorder characterized by elevated blood glucose levels and a marked increase in the risk of cardiovascular disease (CVD). The increased CVD risk is caused by a unique cluster of metabolic abnormalities, including dyslipidemia, hypertension, insulin resistance, and hyperglycemia. To reduce the risk of cardiovascular complications in patients with type 2 diabetes, comprehensive management of risk factors is essential. Aggressive treatment of dyslipidemia and hypertension is known to benefit patients with type 2 diabetes. In addition, intensive glycemic control and targeted treatment of insulin resistance can further reduce the enormous burden of CVD in this high-risk population. Increasing evidence suggests that insulin resistance is one of the earliest markers of risk for both CVD and diabetes, and it is known that insulin resistance alone can significantly increase the risk of CVD. Type 2 diabetes and insulin resistance are both associated with disordered lipid metabolism, manifest in elevated triglyceride levels, low levels of high-density lipoprotein cholesterol, and small, dense low-density lipoprotein cholesterol particles. Patients with type 2 diabetes and insulin resistance have an increased risk of hypertension, which further contributes to their CVD risk. Each of these factors can also contribute to the risk of microvascular disease. To ensure that patients with type 2 diabetes receive comprehensive, high-quality care, specific standards have been developed. These standards can help providers establish clear treatment targets, identify specific priorities of care, and use therapies of known efficacy to reduce the risk of complications. This review summarizes the current standards of care for patients with type 2 diabetes, with an emphasis on treatments that reduce the cardiovascular risk factors. Using a case study approach, it reviews the essential components of diabetes care and proposes a rational approach to these complex cases--an approach that should result in consistent, high-quality care.
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PMID:Comprehensive management of patients with type 2 diabetes: establishing priorities of care. 1151 98

Insulin resistance is a metabolic disorder that is increasing worldwide and is associated with some of the most common diseases affecting modern societies including diabetes, hypertension, obesity and coronary heart disease. Although pharmacologic approaches to managing insulin resistance are being advocated by some, public health approaches involving changes in diet and physical activity are attractive because of their lower cost and risk. We briefly summarize some new information on the mechanisms that mediate insulin's many biological actions and examine the effects of dietary carbohydrates on insulin sensitivity. Specifically, we summarize some of the information available on the effects of simple sugars, complex carbohydrates including fiber, slowly digested starch and the general concept of glycemic index. The available data support the idea that consumption of diets high in total carbohydrate does not adversely affect insulin sensitivity compared with high fat diets. Animal data suggest that simple sugars, in particular fructose, have adverse effects on insulin action, but adverse effects have not been shown conclusively in humans. Increased intake of dietary fiber appears to improve insulin action and may protect against the development of diabetes. The effects of diets with high or low glycemic index on insulin action are controversial at this time. For firm conclusions to be reached, future studies must be of reasonable duration, be in defined populations and compare the effects of relevant doses of nutrients on specific endpoints of insulin action.
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PMID:The role of carbohydrates in insulin resistance. 1158 6

Although diabetes mellitus is predominantly a metabolic disorder, recent data suggest that it is as much a vascular disorder. Cardiovascular complications are the leading cause of death and disability in patients with diabetes mellitus. A number of recent reports have emphasized that many patients already have atherosclerosis in progression by the time they are diagnosed with clinical evidence of diabetes mellitus. The increased risk of atherosclerosis and cardiovascular complications in diabetic patients is related to the frequently associated dyslipidemia, hypertension, hyperglycemia, hyperinsulinemia, and endothelial dysfunction. The evolving knowledge regarding the variety of metabolic, hormonal, and hemodynamic abnormalities in patients with diabetes mellitus has led to efforts designed for early identification of individuals at risk of subsequent disease. It has been suggested that insulin resistance, the key abnormality in type II diabetes, often precedes clinical features of diabetes by 5-6 years. Careful attention to the criteria described for the cardiovascular dysmetabolic syndrome should help identify those at risk at an early stage. The application of nonpharmacologic as well as newer emerging pharmacologic therapies can have beneficial effects in individuals with cardiovascular dysmetabolic syndrome and/or diabetes mellitus by improving insulin sensitivity and related abnormalities. Early identification and implementation of appropriate therapeutic strategies would be necessary to contain the emerging new epidemic of cardiovascular disease related to diabetes.
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PMID:Clinical significance of cardiovascular dysmetabolic syndrome. 1198 76

Obesity is a major contributor to the prevalence of cardiovascular disease in the developed world, and yet has only recently been afforded the same level of attention as other risk factors of coronary artery disease. Obesity is a chronic metabolic disorder associated with cardiovascular disease and increased morbidity and mortality. It is apparent that a variety of adaptations/alterations in cardiac structure and function occur as excessive adipose tissue accumulates, even in the absence of comorbidities. Shifts toward a less physically demanding lifestyle are observed today throughout different populations, and this scourge associated with obesity implicates a corresponding increase in the number of individuals afflicted with the metabolic syndrome, which defines the obese patient as being "at risk." Adipose tissue is not simply a passive storehouse for fat, but an endocrine organ that is capable of synthesizing and releasing into the bloodstream a variety of molecules that may impact unfavorably the risk factor profile of a patient. Indeed, obesity may affect atherosclerosis through unrecognized variables and risk factors for coronary artery disease such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, and the prothrombotic state. By favorably modifying lipids, decreasing blood pressure, and decreasing levels of glycemia, proinflammatory cytokines, and adhesion molecules, weight loss may prevent the progression of atherosclerosis or the occurrence of acute coronary syndrome events in the obese high-risk population.
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PMID:Obesity and cardiovascular disease. 1236 92

The insulin sensitivity in hypertensive patients with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM) and the insulin resistance (IR) under the disorder of glucose metabolism and hypertension were studied. By glucose tolerance test and insulin release test, insulin sensitivity index (ISI) and the ratio of area under glucose tolerance curve (AUCG) to area under insulin release curve (AUCI) were calculated and analyzed. The results showed that ISI was decreased to varying degrees in the patients with hypertension, the mildest in the group of NGT with hypertension, followed by the group of IGT without hypertension, the group of IGT with hypertension and DM (P = 0). There was very significant difference in the ratio of AUCG/AUCI between the hypertensive patients with NGT and controls (P = 0). It was concluded that a significant IR existed during the development of IGT both in hypertension and nonhypertension. The increase of total insulin secretion (AUCI) was associated with nonhypertension simultaneously. IR of the hypertensive patients even existed in NGT and was worsened with the deterioration of glucose metabolism disorder, but the AUCI in the HT group changed slightly. A relative deficiency of insulin secretion or dysfunction of beta-cell of islet existed in IGT and DM of the hypertensive patients.
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PMID:Insulin resistance and hypertension. 1267 74

Trimethylaminuria is a rare metabolic disorder that is associated with abnormal amounts of the dietary-derived trimethylamine. Excess unmetabolized trimethylamine in the urine, sweat and other body secretions confers a strong, foul body odor that can affect the individual's ability to work or engage in social activities. This review summarizes the biochemical aspects of the condition and the classification of the disorder into: 1) primary genetic form, 2) acquired form, 3) childhood forms, 4) transient form associated with menstruation, 5) precursor overload and 6) disease states. The genetic variability of the flavin-containing monooxygenase (form 3) that is responsible for detoxication and deodoration of trimethylamine is discussed and put in context with other variant forms of the flavin-containing monooxygenase (forms 1-5). The temporal-selective expression of flavin-containing monooxygenase forms 1 and 3 is discussed in terms of an explanation for childhood trimethylaminuria. Information as to whether variants of the flavin-containing monooxygenase form 3 contributes to hypertension and/or other diseases are presented. Discussion is provided outlining recent bioanalytical approaches to quantify urinary trimethylamine and trimethylamine N-oxide and plasma choline as well as data on self-reporting individuals tested for trimethylaminuria. Finally, trimethylaminuria treatment strategies and nutritional support are described including dietary sources of trimethylamine, vitamin supplementation and drug treatment and issues related to trimethylaminuria in pregnancy and lactation are discussed. The remarkable progress in the biochemical, genetic, clinical basis for understanding the trimethylaminuria condition is summarized and points to needs in the treatment of individuals suffering from trimethylaminuria.
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PMID:Biochemical and clinical aspects of the human flavin-containing monooxygenase form 3 (FMO3) related to trimethylaminuria. 1267 93

Although a salted diet appears to be a sine qua non for the development of essential hypertension, low-salt diets often have a modest or even negligible impact on the blood pressure of hypertensives; this suggests that salt, perhaps often acting in concert with other aspects of a modern, rich diet, may set in place certain metabolic vicious cycles that sustain blood pressure elevation even when dietary salt is eliminated. Therapeutic fasting is known to lower elevated blood pressure - presumably in large part because it minimizes insulin secretion - and may have the potential to break some of these vicious cycles. Goldhamer has recently reported that a regimen comprised of a water-only fast of moderate duration, followed by a transition to a low-fat, low-salt, whole-food vegan diet, achieves dramatic reductions in the blood pressure of hypertensives, such that the large majority of patients can be restored to normotensive status, in the absence of any drug therapy. Although long-term follow-up of these subjects has been sporadic, the available data suggest that these large reductions is blood pressure can be conserved in patients who remain compliant with the follow-up diet - in other words, a 'cure' for hypertension may be feasible. If a protein-sparing modified fast can be shown to be virtually as effective as a total fast for achieving these benefits, it may be possible to implement this regimen safely on an outpatient basis. The ability of therapeutic fasts to break metabolic vicious cycles may also contribute to the efficacy of fasting in the treatment of type 2 diabetes and autoimmune disorders. As a general principle, if a metabolic disorder is susceptible to prevention - but not reversal - by a specific diet, and therapeutic fasting has a temporary favorable impact on this disorder, then a more definitive therapy may consist of a therapeutic fast, followed up by the protective diet as a maintenance regimen.
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PMID:A preliminary fast may potentiate response to a subsequent low-salt, low-fat vegan diet in the management of hypertension - fasting as a strategy for breaking metabolic vicious cycles. 1271 Aug 93


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