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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present status of knowledge about glucagon pathophysiology in diabetes is reviewed. 1) A-cells behave abnormally in all varieties of diabetes mellitus, spontaneous and experimental, except perhaps in case of pancreatectomized humans. These abnormalities are : hyperreactivity of A-cells to arginine, non suppressibility by glucose, and absence of stimulation following hypoglycemia. 2) These abnormalities appear as secondary in most instances : a) A-cells behave in a normal way in most studies with prediabetics ; b) plasma glucagon concentration is normalized by excellent control of diabetes or following prolonged insulin infusion. High doses of insulin are required most of the times to obtain a normalization of A-cell function : in insulin-dependent diabetics, the physiological portoperipheral insulin gradient no longer exists, and the high doses of insulin which are necessary may be the only mean to reconstitute the high insulin concentrations supposed to be present at the A-cell level. 3) Conflicting results have been collected about the role of this glucagon excess in aggravating the diabetic metabolic syndrome. Evanescent effects follow sustained glucagon infusions: but in diabetics, glucagon bursts rather than permanent hyperglucagonemia are observed and these appear deleterious to glucose tolerance. It seems clear however that insulin deprivation is required for the full expression of the consequences of glucagon excess.
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PMID:Glucagon and diabetes mellitus. 37 65

With the help of data from literature and own long-term observations the importance of the hyperlipoproteinaemias (HLP type IIb-V) as precursors of the maturity-onset-diabetes is discussed. The assumption of transitions of the hyperlipoproteinaemias with insignificant disturbances of the carbohydrate tolerance and hyperinsulinism into a condition with manifest diabetes mellitus and relative lack of insulin appears justified. Differential diagnostics (e.g. by determination of the insulin response after glucose tolerance) and adequate differential therapy of the symptom complex belonging to the metabolic syndrome are demanded.
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PMID:[Hyperlipoproteinemia -- cause or sequelae of maturity-onset diabetes]. 119 46

It is well known that excessive weight is associated with resistance to insulin-mediated glucose uptake and predisposition to the development of type II diabetes. It has been shown more recently that excessive weight and insulin resistance tend to be associated to android fat distribution, arterial hypertension, elevated levels of triglycerides, low concentration of HDL cholesterol and defective fibrinolysis. The terms syndrome of insulin resistance, metabolic syndrome or syndrome X have been proposed to describe this cluster of abnormalities. The pathophysiological mechanisms which could explain the interrelations between these different parameters are still only partly understood. Epidemiological prospective studies have demonstrated that the metabolic syndrome is a risk factor for coronary heart disease and type II diabetes. The mechanisms involved in the development of diabetes are relatively well established, but those which are implicated in the atherothrombotic process are far from being clearly described. Anyway, sufficient presumption exists to attempt at decreasing insulin resistance when it exists. Physical training and, if indicated, weight reduction are the simplest means.
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PMID:The syndrome of insulin resistance. 130 11

Hypertension has previously been suggested to be a part of a metabolic syndrome also involving hyperlipidemia, hyperinsulinemia, and decreased insulin sensitivity. In the present study, 10 untreated hypertensive subjects were challenged with a high-salt diet (20 g NaCl) for 1 week after 7 days on a low-salt diet (less than 3 g). The difference in mean blood pressure (MBP) at the end of the high-salt diet v the low-salt diet was denoted salt sensitivity. We related the salt sensitivity to indices of glucose and lipid metabolism and studied the effect of salt deprivation on these metabolic variables. Salt sensitivity was found to be significantly correlated to HDL cholesterol (r = 0.79, P less than .007), insulin sensitivity (M value at the euglycemic clamp, r = 0.68, P less than .003), and fasting serum insulin (r = 0.69, P less than .04). Salt deprivation induced an increase in fasting insulin (P less than .03), but did not significantly affect any other indices of glucose and lipid metabolism. In conclusion, our study shows that hyperinsulinemia, decreased sensitivity to insulin, and low levels of HDL cholesterol were most commonly seen in hypertensive subjects with a low sodium sensitivity. A putative mechanism might be an increased activity in pressor systems also affecting glucose and lipid metabolism.
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PMID:Metabolic cardiovascular risk factors and sodium sensitivity in hypertensive subjects. 138 59

A double-blind, placebo-controlled, cross-over study was carried out in 25 healthy, nonobese middle-aged men to test the effect of guar gum on glucose and lipid metabolism, blood pressure, and fibrinolysis. Ten grams guar or placebo granulate was given three times a day for 6 wk with a 2-wk run-in before and a wash-out period after. Decreases in fasting blood glucose (P < 0.001), cholesterol (P < 0.001), triglycerides (P < 0.05), plasminogen activator inhibitor-1 activity (P < 0.01), systolic blood pressure (P < 0.01), and diastolic blood pressure (P < 0.001) were seen during guar treatment when compared with placebo. Insulin sensitivity, measured with the euglycemic-clamp technique, increased (P < 0.01), adipose tissue-glucose uptake measured in vitro increased (P < 0.001), and 24-h urinary excretion of sodium and potassium increased (P < 0.001) during guar treatment. Fasting plasma insulin, renin, aldosterone, and fibrinogen concentrations as well as skeletal-muscle electrolytes, urinary catecholamines, and body weight remained unaltered. These findings support a role for guar in the treatment of the metabolic syndrome in which insulin resistance seems to play a pivotal role.
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PMID:Guar gum improves insulin sensitivity, blood lipids, blood pressure, and fibrinolysis in healthy men. 144 58

A clustering of metabolic disturbances has been indicated in hypertension. The distribution of such factors was assessed among hypertensives and normotensives in a general population sample of 644 men aged 67 years. Fasting serum insulin, glucose and triglyceride levels were measured. In this study hypertension was defined as DBP > or = 95 mmHg or present use of antihypertensives. Impaired glucose tolerance (IGT) or diabetes mellitus, hyperinsulinaemia (> or = 20 mU l-1) and hypertriglyceridaemia (> or = 2.3 mmol l-1) were defined as metabolic disturbances. When all these disturbances were present simultaneously a complete 'metabolic syndrome' was considered to be present. Hypertension was found in 185 (29%) men, IGT in 15%, diabetes mellitus in 11%, hyperinsulinaemia in 18% and hypertriglyceridaemia in 19%. Among hypertensives, 11 (6%) men had a 'metabolic syndrome', compared to 12 (3%) men in the normotensive group (P = 0.039). At least one metabolic disturbance was present in 109 (59%) of the hypertensive men, and in 173 (38%) of the normotensive men (P < 0.001). The prevalence rates of metabolic disturbances did not differ significantly between lean (BMI < 26 kg m-2) and obese (BMI > or = 26 kg m-2) hypertensives. Only hypertriglyceridaemia was more frequent in obese than in lean hypertensives (20% vs. 37%, P = 0.015). The 'metabolic syndrome' was found in 6% of all hypertensives, which was twice as common as in the normotensive population. The 'metabolic syndrome' was uncommon in both lean and obese hypertensives (5% vs. 7%, NS). These findings indicate that hypertension and metabolic disturbances may have a common underlying cause, at least in some individuals.
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PMID:Metabolic disturbances in hypertension: results from the population study 'men born in 1913'. 145 22

Today, essential hypertension is considered to be genetically closely related to disordered peripheral glucose metabolism, and this situation is described by the term metabolic syndrome. Both diseases--hypertension and type II diabetes--submit the heart and arterial vessels to an unphysiological, chronic stress, which they can compensate only for a certain time. Today, when antihypertensive treatment is indicated, drugs capable of preventing late vascular injury while at the same time having the potency to reverse already existing organic changes, are employed. ACE-inhibitors are presently considered to be the most potent substances that are capable of exerting a positive effect on hypertension-associated changes, while not increasing the individual risk profile in the development of arteriosclerosis. The present paper discusses the new ACE-inhibitor, cilazapril, which can be administered in a practical single dose and develops a profile of action typical of ACE-inhibitors in hypertensives with and without an accompanying metabolic syndrome.
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PMID:[ACE inhibition with cilazapril. Major therapeutic aspects: hypertension and metabolic syndrome]. 147

The metabolic syndrome (syndrome X) is characterised by an association of elevated insulin levels, a tendency to obesity of the android type, a disturbance of lipid metabolism with elevated triglyceride levels and commonly associated hypertension. The underlying common cause of this syndrome appears to be insulin resistance of the skeletal muscles, which is related in particular to the non-oxidative glucose utilization on the part of the muscle. The molecular cause of this syndrome has not been clarified, but a defect in the signal transduction chain between the insulin receptor and glycogen synthase is suspected. Epidemiological studies have shown that the metabolic syndrome may be considered a preliminary stage of manifest type II diabetes. In addition, it appears to play a major role in the development of cardiovascular complications in certain high-risk groups.
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PMID:[Pathophysiologic principles of metabolic syndrome. Consequences for early diagnosis and prevention]. 148 14

Insulin resistance associated with hyperinsulinemia (metabolic syndrome) emerged in recent years as an important health risk which is present in approximately 25% of the normal population in western industrialized societies. Insulin resistance as assessed for the whole body arises from a reduced glucose utilization of skeletal muscle. If the metabolic syndrome persists over a prolonged period of time, detrimental influences on the cardiovascular system become apparent involving diabetes mellitus, hypertension, and arteriosclerosis. Of particular pathogenic relevance is an unbalanced influence of insulin arising either from a diminished or enhanced insulin action depending on whether the various tissues of the body exhibit a reduced or unchanged insulin sensitivity. Since insulin resistance and hyperinsulinemia appear to be affected by various lifestyle factors, the unique opportunity exists of reducing cardiovascular mortality by correcting this syndrome at a time when degenerative changes have not occurred in the cardiovascular system. Of great importance is the finding that dietary factors can have a modulatory action on insulin sensitivity. In animal experiments, an increased intake of (saturated) fat and refined carbohydrates increased insulin resistance. Since psychosocial distress is expected to be associated with a sustained activation of the sympathoadrenal axis, it is likely also to aggravate the metabolic syndrome. A factor with a beneficial action appears to be physical exercise. In view of the high incidence of cardiovascular diseases, further research on lifestyle factors with an insulin-sensitizing or insulin-desensitizing action is required. Of prime importance is the reevaluation of established dietary recommendations and diets should be designed which take into account the individual cardiovascular risk factor profile.
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PMID:Insulin resistance, hyperinsulinemia, and cardiovascular disease. The need for novel dietary prevention strategies. 159 Jul 42

Epidemiological studies have clearly shown that the so-called metabolic syndrome which is linked to insulin resistance and a reduced glucose utilization of muscle represents an important risk factor for cardiovascular disease. However, only little is known of the intracellular consequences of insulin resistance. An important feature of an altered substrate utilization is related to signal transduction of gene expression. For the example of myosin heavy chain expression, it is shown that metabolic signals exist which reflect the fuel flux and substrate utilization of the heart muscle cell. The signals were characterized in functional states of the heart associated with altered metabolic influences (fasting, diabetes, sucrose feeding, increased calorie intake, carnitine palmitoyltransferase inhibition). In the pressure-overloaded heart, metabolic interventions which are expected to increase glucose utilization (sucrose feeding, captopril treatment) have a pronounced effect. Although a link with gene expression remains to be established, it should be noted that the sarcoplasmic reticulum Ca(2+)-pump activity seems to be affected in a functionally comparable manner. It is concluded that metabolic signals alter the protein phenotype of heart muscle and it is expected that a deranged signal transduction affects, not only the heart, but also vascular muscle.
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PMID:The metabolic syndrome and signal transduction of gene expression. 183 54


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