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Metabolic syndrome is a clustering of many insulin resistance-associated cardiovascular risk factors such as hypertension, hypertriglyceridaemia, low high-density lipoprotein (HDL) cholesterol, abnormal glucose metabolism and hyperinsulinaemia. Furthermore, it is known that obesity is the most common clinical state characterized by insulin resistance. Central adiposity, in particular, has been shown to be the most distinctive feature of this syndrome. Some studies have also suggested that obesity per se would be necessary for the expression of metabolic defects associated with centrally distributed fat. It has been presented that undernutrition in utero might 'programme' blood pressure, insulin resistance, blood coagulation and cholesterol metabolism and would thus have a role in the aetiology of cardiovascular disease and type 2 diabetes in adult life. Some studies have also found associations between low birthweight and metabolic syndrome in adulthood. However, criticism on this hypothesis of fetal programming has recently been presented. It has been suggested that the origins of adulthood risk of cardiovascular disease and type 2 diabetes can be related to somatic growth as a child, not necessarily to intrauterine growth. In westernized countries, the relative proportion of underweight newborn children is decreasing, and thus considering entire populations low birthweight has lost its theoretical role in the aetiology of type 2 diabetes and cardiovascular disease. On the other hand, as obesity is known to be increasing in the industrialized countries among all age groups, the association between weight gain in childhood and metabolic syndrome in adulthood is more than noteworthy. Instead of undernutrition during pregnancy, sedentary lifestyle and lack of physical exercise pose a new threat. This results in an increased occurrence of overweight in childhood, which may be the first sign of insulin resistance and future metabolic syndrome.
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PMID:Childhood weight and metabolic syndrome in adults. 1048 Jul 53

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

The purpose of this study was to examine characteristics associated with the insulin metabolic syndrome, including insulin resistance, abnormal glucose tolerance, dyslipidemia, obesity, and elevated blood pressure, among women who have experienced gestational diabetes. 39 nondiabetic, young (20-42 years), postpartum (3-18 months) white women were recruited from obstetrical clinics. Twenty-one women had a history of gestational diabetes; 18 had uncomplicated pregnancies. Multivariate analyses revealed a significant difference between groups in insulin resistance (M, measured by euglycemic clamp) and insulin levels (from an oral glucose tolerance test), with insulin resistance showing a statistically stronger difference than insulin levels. Groups also differed significantly when compared on a set of variables associated with insulin metabolic syndrome: glucose tolerance, triglycerides, blood pressure, and body-mass index. Using insulin resistance as a covariate eliminated these group differences, suggesting that insulin resistance is the key factor underlying insulin metabolic syndrome. The higher risk of later developing type 2 diabetes and hypertension in women who have a history of gestational diabetes is explicable by their poorer profile on variables associated with insulin metabolic syndrome, and appears to be attributable to insulin resistance. Thus, insulin resistance appears to distinguish young women at risk for cardiovascular disease.
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PMID:History of gestational diabetes, insulin resistance and coronary risk. 1061 62

The combination of high serum triglyceride levels and small low density lipoprotein particles, with a reduction in high density lipoprotein cholesterol levels has been named atherogenic lipoprotein phenotype or, simply, lipid triad. These lipid factors are commonly associated with peripheral resistance to the action of insulin, hyperinsulinism, central and visceral obesity, hypertension, hyperuricemia, hypercoagulability. The clustering of these nonlipid factors along with the lipid factors has been called metabolic syndrome. Insulin resistance plays a central role in the development of the lipid triad increasing the production of triglyceride-rich lipoproteins and decreasing their catabolism. There is currently great interest about the origins of the metabolic syndrome. One question under considerable research is whether genetic or acquired factors predominate in causing this syndrome. There seems to be little doubt that the metabolic syndrome taken as a whole constitutes a major risk factor for coronary heart disease. What is less certain is that each component of the syndrome is an independent risk factor. People with lipid triad are at very high risk of developing coronary heart disease, and careful management is warranted. Nonetheless, appropriate therapeutic strategies that will modify the metabolic syndrome as a whole are needed. More investigations about key metabolic steps that simultaneously affect multiple pathways will be required to yield a satisfactory therapy for high risk patients exhibiting the metabolic syndrome.
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PMID:[Atherogenic dyslipidemia, metabolic syndrome and cardiovascular risk]. 1063 48

Diabetes mellitus is a complex metabolic syndrome characterised by varying degrees of insulin deficiency, either absolute or relative, and impaired insulin action on protein, lipid and carbohydrate metabolism. Although hyperglycemia is always present during the course of the disease, at least in the early phase it must not be a unique criterion for diagnosis. A normoglycemic patient with hyperinsulinemia associated with obesity or dyslipidemia could be considered as a case of "normoglycemic diabetes" which will develop in time toward hyperglycemia.
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PMID:Proposal for a new classification of diabetes mellitus. 1066 Sep 78

The 'metabolic syndrome' is a special clinical entity characterized by upper body segment obesity (android obesity), together with one or more of a constellation of metabolic disorders that includes glucose intolerance, which may amount to frank diabetes mellitus, hypertension, cardiovascular lesions, hyperuricemia, and dyslipidemias (hypercholesterolemia, hypertriglyceridemia and reduced serum HDL). Recently, lipoprotein (Lp) (a) proved to be a new member in this syndrome. Lp(a) has the distinctive feature of containing apolipoprotein (a), which is a glycoprotein linked to apo B100, and has a similarity to plasminogen; it is also structurally related to LDL. Lp(a) is a macromolecular complex which is genetically determined, and has been identified as an independent risk factor for premature coronary artery disease (CAD). It is elevated in diabetic and non-diabetic android obese subjects, and aggravates the atherogenic effect of diabetes mellitus. Lp(a) is poorly influenced either by dietary measures or by hypolipidemic drugs. Unfortunately, few pharmacologic agents, such as niacin, nicotinic acid, sex hormones (estrogen and testosterone), alcohol and neomycin, affect Lp(a).
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PMID:Lipoprotein (a) in android obesity and NIDDM: a new member in 'the metabolic syndrome'. 1066 39

According to a recent experimental study published in the Lancet, sleep debt, frequently imposed by the life habits of industrialized countries, results in profound metabolic (impaired glucose tolerance) and endocrine (increased sympathetic activity and evening cortisol levels) alterations, which mimic those of normal ageing and may have pathophysiological consequences in the long term. Another study recently published in the International Journal of Obesity demonstrated a significant positive relationship between the duration of shift-work and body mass index or waist to hip ratio, a marker of visceral adiposity. One may thus hypothesize that chronic sleep deprivation could predispose to the metabolic syndrome and increase the cardiovascular risk.
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PMID:[Clinical study of the month. Does chronic sleep deprivation predispose to metabolic syndrome?]. 1066 51

The prevention of cardiovascular diseases relies upon the correction of risk factors and, more particularly, the optimal management of various metabolic abnormalities such as obesity, dyslipidaemias, diabetes mellitus and arterial hypertension. Such an approach first requires the adherence to life-style habits (healthy diet, physical activity and no smoking) and, in case of failure, the use of lipid-lowering drugs, antidiabetic agents and/or antihypertensive medications. Sometimes, a monotherapy may be sufficient but, in most cases, a drug combination is mandatory because of the need to reach tight therapeutic targets and of the presence of a polypathology, especially within the frame of the metabolic syndrome. Unfortunately, all surveys indicate that therapeutic compliance to non-pharmacological advice and even to drug prescriptions is far from being excellent. Such a non-compliance limits the efficacy of the prevention strategies and contributes to markedly increase the cost of metabolic diseases and associated complications.
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PMID:[Therapeutic non-compliance: a major problem in the prevention of cardiovascular diseases]. 1068 96

Serum mannose concentration increases in diabetic patients and correlates closely with blood glucose. In patients with glomerulonephritis, serum mannose and mannose/glucose ratio positively correlate with dyslipidemia and the extent of urinary protein excretion. We investigated whether changes in serum mannose mark subjects with features of metabolic syndrome, including obesity, hypertension, glucose intolerance, and dyslipidemia. The study comprised 20 patients with mean age of 68 (SD 11) years, body mass index 27.2 (SD 5.1) kg/m2, blood glucose 6.2 (SD 1.6) mmol/L, serum total cholesterol 6.3 (SD 1.2) mmol/L, triglyceride 2.0 (SD 0.08) mmol/L, uric acid 320 (SD 109) micromol/L, mannose 60.0 (SD 17) micromol/L, and mannose/glucose ratio 9.7 (SD 1.8) micromol/mmol. Serum mannose correlated with blood glucose (r=0.758, p=0.012), triglyceride (r=0.478, p=0.023), and HDL-cholesterol (r = approximately 0.427, p=0.022). Mannose/glucose ratio correlated with BMI (r=0.581, p=0.033), mannose (r=0.491, p=0.035), and uric acid (r=0.608, p=0.027). The rate of VLDL lipoprotein turnover may be instrumental in the regulation of serum mannose concentration. We conclude that an altered mannose metabolism is a novel consideration among the metabolic abnormalities in the metabolic syndrome.
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PMID:Metabolic syndrome is associated with changes in D-mannose metabolism. 1069 Oct 51

The association between both plasma viscosity and fibrinogen concentration with clustering of metabolic risk markers was examined within a cross-sectional study of employed middle-aged men. Analyses were performed on a subsample of 629 non-smokers (46.7+/-7.8 years) without diabetes. The effect of obesity and cardiorespiratory fitness on these haemorheological parameters and their association with the metabolic syndrome was also investigated. The cohort was grouped by the number of metabolic markers present. Metabolic markers included high-density lipoprotein-cholesterol (<1.13 mmol/l), triglycerides (> or =1.805 mmol/l), glucose (> or =5.5 mmol/l) and diastolic blood pressure (> or =90 mm Hg). The age-adjusted odds ratio for hyperviscosity (> or =1.67 mPa/s) was 2.08 [95% confidence interval (CI), 1.06-4.05; P = 0.031] for the subjects with the metabolic syndrome (three or more metabolic markers) when compared with those with no metabolic abnormalities. The comparable age-adjusted odds ratio for hyperfibrinogenaemia (> or = 3.47 g/l) was non-significantly higher at 1.69 (95% CI, 0.87-3.27; P = 0.119). The mean age-adjusted plasma viscosity level and the prevalence of hyperviscosity increased significantly from 1.629 to 1.692 mPa/s (P = 0.0005) and from 21.0 to 36.0% with accumulating metabolic markers (P = 0.006). Plasma viscosity and fibrinogen concentration both increased with higher quartiles of skinfolds (P = 0.003 and P = 0.01, respectively) following adjustment for age, lipids and leucocyte count. Plasma viscosity was also significantly lower with higher levels of predicted maximum oxygen consumption (VO2max) (P = 0.0005). The odds ratio for hyperviscosity in subjects with the metabolic syndrome as compared with those with no metabolic markers was attenuated following adjustment for age, sum of skinfolds and predicted maximum oxygen consumption (VO2max) (1.44; 95% CI, 0.72-2.90; P = 0.307). These cross-sectional results suggest that plasma viscosity is associated with increased clustering of metabolic markers in middle-aged men of high socio-economic status. Obesity and poor cardiorespiratory fitness may be important in the development of haemorheological abnormalities associated with the metabolic syndrome.
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PMID:Plasma viscosity, fibrinogen and the metabolic syndrome: effect of obesity and cardiorespiratory fitness. 1069 Nov 1


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