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Query: UMLS:C0011849 (diabetes)
 277,896 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

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 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

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


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