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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

Acute arterial occlusions of the extremities may result, in approximately 7.5% of cases, in a severe and complex metabolic syndrome which often leads to loss of limb and life. The manifestations of this syndrome are divided into two stages: (1) the ischemic or devascularization phase, and (2) the revascularization phase. The ischemic phase includes severe clinical manifestations, of which the rigidity of the limb ("rigor mortis") is an outstanding sign, as are nephropathic-metabolic changes (oliguria, acidosis, myoglobinuria, azotemia, hyperkalemia). Their identification and correction at this phase may minimize their impact on the revascularization syndrome. The clinical and metabolic manifestations during the latter phase are more severe and may determine the outcome of the viability of the limb and the survival of the patient. Amputation rates are quite high (40% to 50%) and mortality rates range between 30% and 80%. The ischemic rhabdomyolysis appears to be the initiating event which leads to the biochemical and metabolic alterations that dominate the prognosis as to limb and life. The guiding principles of the management in these severe ischemic cases consist of early revascularization with emphasis on concurrent fasciotomy, alkalinization of the patient, reestablishment of acid-base balance, hemodialysis for renal shutdown, and often early amputation for better control of the metabolic omplications.
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PMID:Muscular, renal, and metabolic complications of acute arterial occlusions: myonephropathic-metabolic syndrome. 43 7

Issuing from the present state of the influence of the basic nutritive substances (protein, fat, carbohydrates) and various nutritive factors discussed again and again (cholesterol, erucaic acid, sodium, calcium/magnesium quotient, pressor amines) on the development of the arteriosclerosis, the indididual factors of influence are critically evaluated. The investigations are getting under way, so that ascertained results are standing beside insufficiently claified or open problems, From the abundance of the observations conclusions are drawn which are of significance for practice. Unfavourable influences of nutrition on the factors of risk (hyperlipoproteinaemia, disturbance of the carbohydrate tolerance, hyperuricaemia, hyperalimentation) and on the manifest diseases (hypertension, diabetes mellitus, uric arthritis, obesity) of the metabolic syndrome which finally contribute to the development of arteriosclerosis are emphasized. In front of this background a clinically and ambulatorily tested basic metabolic diet is described. About 20% of the energy content (kcal or kJ) of this diet are protein, 35% fat and 45% are carbohydrates. The saturated fatty acids lie below 30%, the manifold saturated fatty acids, however, above 20% of the total fat proportion. The cholesterol content is below 400 mg, the purin-nitrogen below 200 mg, and the sodium content is about 2g per day. This diet can be produced for the treatment of persons with normal weight and overweight in different energetic degradations.
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PMID:[Nutrition and arteriosclerosis]. 70

The investigation is realized with 50 diabetics, considered suitable for oral therapy that revealed excellent or satisfactory effect from the Glybenclamide treatment (GCL), applied separately or in combination with butyl biguanide. GCL was established to give far better results than the rest oral antidabetic drugs, permitting a better metabolic syndrome compensation. GCL effect is more manifested than that of tolbutamide. The better therapeutic effect of GCL is obvious as compared with chloropropamide and butyl biguanide, but not so well manifested as with tolbutamide. The therapeutic GCL effect is better in almost all followed up ages, the most advanced incld., which is not cogent for the rest of the oral preparations. Side effects and severe hypoglycemic incidence, reported by other authors, were not observed during the investigation.
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PMID:[Therapeutic effect of glibenclamide contrasted with other oral antidiabetic agents]. 81 18

Seventeen patients with malignant disease developed a complex metabolic syndrome of 2-8 weeks' duration characterized by hypocalcemia, hypomagnesemia and hypokalemia following administration of the aminoglycoside group of antibiotics. Gentamicin, Tobramycin, Amikacin, and Sisomicin were all involved. Other features noted were hypoalbuminemia, hypophosphatemia, and hypouricemia. Low immunoreactive parathyroid hormone (i-PTH) levels in the presence of hypocalcemia and absence of hyperplastic changes in the parathyroid gland examined at postmortem confirmed a diagnosis of hypoparathyroidism. Immunoreactive calcitonin levels (i-CT) were not elevated. Renal tubular wasting of potassium and magnesium was documented in six patients and excessive urinary loss of sodium, phosphate, and uric acid was noticed. Twelve patients died before recovering from the metabolic stress and five patients developed progressive renal impairment. A possible potentiating action of chemotherapeutic agents, especially Adriamycin, is suggested.
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PMID:Hypocalcemia with hypoparathyroidism and renal tubular dysfunction associated with aminoglycoside therapy. 85 39

The diagnostics of hyperlipoproteinaemias is essentially based on the proof of biochemical parameters. The simultaneous determination of triglycerides and cholesterol in the serum is the most important measure for establishing disturbances of the lipid metabolism. The behaviour of these two lipids, the consideration of the serum and the lipoprotein electrophoresis in most cases make possible a classification according to the distributed all over the world and clinically relevant division according to Fredrickson. Loading tests for the early recognition of hyperlipoproteinaemias - analogus to protodiabetes - are hitherto not yet known. Within the diagnostics shoude be taken into consideration that hyperliproproteinaemias are frequently associated with other metabolic diseases (obesity, gout, diabetes mellitus, hypertension) as so-called metabolic syndrome.
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PMID:[Diagnosis of primary hyperlipoproteinemias]. 90 91

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

In form of a survey report the author enters the modern knowledge and opinions concerning the etiopathogenesis of diabetes. Endogenic (hereditary) and exogenic (above all hyperalimentation and malnutrition, deficient muscular conditioning) factors act together. To the functional capacity and functional reserve of the B-cell a central importance is ascribed. The author particularly deals with the possibility of a bihormonal disturbance and with the metabolic syndrome as well as a differentiation into the two most important types of diabetes is performed. As to several problems the results of the Karlsburg team are cited.
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PMID:[Etiopathogenesis of diabetes mellitus today (continuation)]. 122 44

Recent studies have indicated that the waist/hip circumference ratio (WHR), an index of abdominal fat distribution, is a risk factor for cardiovascular disease and diabetes, in parallel with other previously established risk factors. Obesity, without taking fat distribution into account, seems to be associated with WHR in its relationship to the metabolic risk factors for these diseases. The important component of the WHR is probably the mass of visceral fat. This cluster of phenomena constitute what has recently been called the metabolic syndrome or syndrome X. Visceral fat mass is probably increased by a multiple endocrine aberration, where steroid hormones are important. This seems to cause insulin resistance by direct effects on the periphery, which may be amplified by the metabolism of the enlarged visceral adipose tissues.
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PMID:Abdominal fat distribution and the metabolic syndrome. 128 66

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


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