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The precise molecular cause of insulin resistance has not yet been elucidated. Resistance to the normal action of insulin contributes to the pathogenesis of a number of common human disorders, including type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus, hypertension, and the Metabolic Syndrome X, thus constituting a major public health problem. A disease program aimed at combating this disorder should focus on the identification of targets for therapeutic intervention which may overcome insulin resistance and hence the associated metabolic consequences characteristic of the Metabolic Syndrome. Although the primary defect in the pathogenesis of type 2 diabetes is unknown, genetic and environmental factors are likely to contribute to the manifestation of this progressive metabolic disorder, which is usually not clinically apparent until mid-life. Defects at the level of glucose uptake/phosphorylation characterize insulin resistance in skeletal muscle of type 2 diabetic patients. Identification of putative components of the insulin receptor-signaling pathway may offer insights into mechanisms involved in insulin resistance. Enhanced flux of free fatty acids due to impaired lipid metabolism may contribute to impaired insulin secretion and peripheral insulin resistance. Genes regulating lipolysis are prime candidates for susceptibility towards the metabolic syndrome. Here we describe pathways constituting complex interactions that control glucose homeostasis. We will be considering (1) regulation of glucose uptake by the insulin receptor signaling pathway, and (2) control of adipogenesis and insulin sensitivity by the sterol response element binding protein (SREBP) pathway.
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PMID:Analysis of insulin signaling pathways through comparative genomics. Mapping mechanisms for insulin resistance in type 2 (non-insulin-dependent) diabetes mellitus. 1284 56

Diabetic patients develop atherosclerosis in an accelerated way as compared to non-diabetic patients. This is due to a generalized metabolic disorder that includes hyperglycemia, insulin resistance, dyslipidosis, loss of the endothelial regulatory function, a tendency for vasoconstriction, and a prothrombotic state. The main complications are coronary artery disease, peripheral vascular disease, and cerebrovascular disease. In all these manifestations and at all severity levels, diabetic patients, in particular post-menopausal women, have the worst prognosis with any type of treatment as compared to non-diabetic patients. These findings lead to consider the sole presentation of diabetes mellitus to be equivalent to cardiovascular risk. The largest reduction in risk is achieved by controlling hypertension, followed by a control of glycemia, reduction of glycosylated hemoglobulin and control of dyslipidosis. Benefits in the cardiovascular realm have not extended to other vascular territories, such as the lower extremities or the brain.
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PMID:[Control of atherosclerosis in diabetes mellitus]. 1296 62

Type 2 diabetes mellitus is a major health problem associated with excess morbidity and mortality. Defects in the action and/or secretion of insulin are the two major abnormalities leading to development of glucose intolerance. Any intervention in the impaired glucose tolerance phase that reduces resistance to insulin or protects the beta-cells, or both, should prevent or delay progression to diabetes. The natural history of type 2 diabetes includes a preceding period of impaired glucose tolerance (IGT)/impaired fasting glucose (IFG) which provides an opportunity for targeted intervention within large communities. As the prevalence of this metabolic disorder is rapidly increasing and current treatment fails to stabilise the disease in most patients, prevention should be considered as a key objective in the near future. Lifestyle intervention studies have consistently shown that quite modest changes can reduce the progression from IGT to diabetes by 50-60%. The Diabetes Prevention Program (DPP) randomised trial has shown that a combined program of weight loss, improvement of diet and increase of physical exercise lowers the risk for development of type 2 diabetes by 58% compared with placebo. It may, however, not be possible to translate these successful findings to larger cohorts or maintain the lifestyle changes longer term. This has lead to consideration of pharmacotherapy. Benefits have been found for metformin, acarbose and troglitazone. Treatment with metformin was less effective than lifestyle modifications, resulting in an average reduction of risk for development of type 2 diabetes by 31% compared with placebo. Similarly, acarbose in the STOP-NIDDM trial reduced the risk of developing type 2 diabetes in patients with IGT by 25%. Remarkably, cardiovascular event rates, in particular myocardial infarction, were significantly reduced when acarbose was used instead of placebo in subjects with glucose intolerance. The ACE inhibitors captopril (CAPPP) or ramipril (HOPE) and the Angiotensin-II receptor antagonist losartan (LIFE) have been shown to reduce the appearance of diabetes by one third when given to patients with hypertension. Since many hypertensive patients are insulin-resistant and have an increased risk in developing type 2 diabetes, the protective effect of these classes of antihypertensive drugs might be explained by their antiinsulin-resistance effects.
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PMID:[Progress in the prevention of type 2 diabetes]. 1474 78

Precocious admission to specifically "dedicated" wards proved to improve reduction of mortality and degree of residual disability in patients with stroke, even if their inhomogeneous distribution gets most patients admitted to wards of Internal Medicine. We purposed to evaluate the importance of this problem, to check adhesion to the national guidelines and to show the main problems in management of patients with stroke in the Operative Unit of Internal Medicine, Vascular and Metabolic Diseases of the IRCCS S. Matteo Hospital of Pavia. 143 patients with stroke were admitted in 2001, 126 were ischemic, 17 hemorragic; the mean age was of 73. The most frequent risk factors were hypertension, diabetes, smoke and atrial fibrillation. 59% of patients were admitted within 6 hours from onset of symptoms. Within the ischemic subtypes, 17.5% were atherotrombothic, 16.7% cardioembolic, 23.8% lacunar and 42% with undetermined etiology. Lacunar syndromes were the most part. 80% of patients underwent computed tomography, 50% underwent epiaortic Doppler sonography, 38% echocardiography. 61% of ischemic subtypes underwent acute antiplatelet treatment. Complications were prevalent in oldest patients. Mortality of inpatients was 17%, influenced by age, hypertension, severe sensorial compromission at admission, cardioembolism and complications. This study proved leak of adhesion to national guidelines which brought to inadequate accuracy in diagnosis and difficulty in making correct and coherent therapeutic choices. At least in great hospitals, "dedicated" areas in wards of Internal Medicine with selected, trained and motivated staff should be desirable.
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PMID:[Management of stroke in a ward of internal medicine. Limits and prospects]. 1514 49

Insulin resistance is a progressive metabolic disorder associated with inactivity, ageing, genetic predisposition and environmental factors, and is a hallmark feature of a variety of disease states including obesity, dyslipidemia, hypertension, polycystic ovarian syndrome, arteriosclerosis and noninsulin dependent (Type 2) diabetes mellitus. The primary defect in the development of whole body insulin resistance remains unclear. However, during the past decade major advances have been made in our understanding of the molecular and cellular mechanisms regulating the entry of glucose into insulin-sensitive tissues. Such an understanding is critical in the identification of specific glucoregulatory biochemical/molecular sites that can be targeted by treatment strategies (i.e. exercise training) in the prevention and treatment of insulin resistance. The five papers comprising this symposium provide a state-of-the-art synopsis of the metabolic, cellular, and molecular mechanisms positively affected by exercise training in individuals who are insulin resistant.
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PMID:Introduction-preventing insulin resistance through exercise: a cellular approach. 1523 23

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.
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PMID:[Scuba diving and the heart. Cardiac aspects of sport scuba diving]. 1524 40

In the presence of a clinical acute monoarthritis, a differential diagnosis has to be made between septic arthritis, gout and diffuse chondrocalcinosis. Gout comes from a purine nucleotide metabolism disorder leading to serum urate level elevation. This hyperuricemia can lead to the deposition of monosodium urate crystals in the joints, causing acute attacks. After long-term evolution, others tissues as the kidneys can be involved: it is chronic gout. The definite diagnosis is based on the presence of monosodium urate crystals in the joint fluid. The diagnosis of gout should prompt a search for associated medical conditions that may affect both urate levels and longevity. These include alcoholism, various nephropathies, myeloproliferative disorders, and hypertension.
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PMID:[Gout]. 1526 76

Obesity is a common and serious metabolic disorder in the developed world that is occasionally accompanied by type II diabetes, atherosclerosis, hypertension, and hyperlipidemia. We have found that mesoderm-specific transcript (Mest)/paternally expressed gene 1 (Peg1) gene expression was markedly enhanced in white adipose tissue of mice with diet-induced and genetically caused obesity/diabetes but not with streptozotocin-induced diabetes, which does not cause obesity. Administration of pioglitazone, a drug for type II diabetes and activator of peroxisome proliferator-activated receptor (PPAR)gamma, in obese db/db mice reduced the enhanced expression of Mest mRNA in adipose tissue, concomitant with an increase in body weight and a decrease in the size of adipose cells. Ectopic expression of Mest in 3T3-L1 cells caused increased gene expression of adipose markers such as PPARgamma, CCAAT/enhancer binding protein (C/EBP)alpha, and adipocyte fatty acid binding protein (aP)2. In transgenic mice overexpressing Mest in adipose tissue, enhanced expression of the adipose genes was observed. Moreover, adipocytes were markedly enlarged in the transgenic mice. Thus Mest appears to enlarge adipocytes and could be a novel marker of the size of adipocytes.
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PMID:Mest/Peg1 imprinted gene enlarges adipocytes and is a marker of adipocyte size. 1535 8

Metabolic syndrome also can be named insulin resistance syndrome. The main clinical manifestations include metabolic disorders of glucose and lipid and some diseases caused by the metabolic disorder, such as impaired glucose tolerance or diabetes, obesity, hyperlipemia, fatty liver, hypertension, coronary heart disease, microalbuminuria, etc. According to the theory of zang-fu organs (viscera) in traditional Chinese medicine, these diseases all result from the deficiency of spleen-qi. They are characterized by deficiency in the Ben (root) and excess in the Biao (branch). The Ben (root) is the failure of the spleen in transportation, and the Biao (branch) is stagnation of qi, blood, phlegm, fire, dampness and food. In the prevention and treatment of metabolic syndrome, it is advocated that the intervention of medicine should be used as early as possible, so as to slow down the occurrence and development of insulin resistance, and that emphasis should be transferred from decreasing blood glucose alone to comprehensive prevention of risk factors, especially to the prevention of cardiovascular events. The effect of traditional Chinese herbs is not as good as the western drugs in decreasing the blood pressure and glucose. However, the traditional Chinese herbs have distinctive superiority in ameliorating the insulin resistance, protecting the injury of vascular endothelial cells, regulating the metabolism of lipid, inhibiting the hypercoagulability, and treating the inflammation. Moreover, they are relatively safe. Therefore, the integration of the traditional Chinese medicine and western medicine is worth further research.
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PMID:[Prevention and treatment of metabolic syndrome with integrated traditional Chinese and western medicine]. 1538 69

Erectile dysfunction (ED) is 2-3 times more frequent in men with diabetes mellitus than in men without such a history and might be an early marker of endothelial dysfunction. We studied a group of 310 unselected male patients within the Clinical Center of Diabetes and Metabolic Diseases of Dolj County, with ages ranging between 20-78 years (57.43 + 0.835) and a positive history of diabetes mellitus for 1-47 years (10.09 +/- 8.715). Erectile dysfunction, quantified using SHIM (Sexual Health Inventory for Men), was present in 196 patients (63.2%); severe in 52 patients (16.8%), moderate in 42 patients (13.5%) and mild in 102 patients (32.9%). Erectile dysfunction showed a positive correlation with age after 65 years, history of diabetes of more than 10 years, obesity, stroke, arteriopathy, retinopathy, neuropathy and the smoking habit and was not correlated to the type of diabetes mellitus, history of diabetes less than 10 years, diabetes therapy, hypertension, ischemic heart disease, nephropathy, dyslipidemia and alcohol consumption. Our results plead for a holistic approach of the diabetic patient, irrespective of age, in order to detect and to treat all the risk factors, keeping in mind that the appearance of erectile dysfunction might indicate the presence of occult chronic diabetes complications.
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PMID:Erectile dysfunction in diabetes mellitus. 1552 1


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