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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapy of gout is discussed taking into consideration the concomitant diseases occurring significantly frequently in patients with gout: Hypertension, uric acid-nephrolithiasis, hyperlipoproteinaemia, obesity, premature arteriosclerosis as well as diabetes mellitus. In contrast to other opinions the authors are of the opinion that the dietetic treatment is furthermore of essential importance. It is referred to the still allowed sufficiently great number in the supply of nourishment, in which cases, however, the limitations in the supply of calories, protein or purin bodies, respectively, lipid and carbohydrate do not remain unmentioned. The propositions for the medicamentous treatment essentially correspond to the central therapeutic recommendations. For the acute attack of gout, however, following to the international experiences, the colchicine therapy is more emphasized again. The medicamentous therapy of the asymptomatic hyperuricaemia is to be included into the considerations after full exhaustion of all dietetic and other possibilities in constant increase of the serum-uric acid-level more than 8 mg/dl.
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PMID:[Therapy of gout]. 33 84

Complex clinical and laboratory research of nonspecific immunobiological reactivity was conducted in 86 children (35 with diabetes mellitus, 25 with obesity, and 26 healthy children), aged from 3 to 14 years. Lysozyme activity and complement titre were studied during the disease. Reduced reactive possibilities of the organism were demonstrated in diabetic children; reduction of these parameters was directly proportional to the severity of the main process and the extent of decompensation. In obese patients the parameters of nonspecific reactivity tests were higher than in healthy children, and glucose tolerance was disturbed; this was apparently connected with stress of the compensatory-defense mechanisms of the organism. A distinct reduction of the parameters in this group of children under the effect of unfavourable factors pointed to exhaustion of the compensatory mechanisms. Obese patients should be referred to the group of children will increased risk, both in respect to diabetes mellitus and to other diseases. The indices under study could be applied as tests characterizing not only the immunobiological reactivity and the defense-adaptive mechanisms of the organism, but also the severity and phase of the disease.
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PMID:[Comparison of the clinical and immunological indices in children with diabetes mellitus and obesity]. 42 86

The conception of a specific association between maturity-onset diabetes and manic-depressive psychosis, on a common basis with diencephalic functional obesity, has been recently taken again in consideration by the psychiatric literature. Investigations on this problem from diabetological point of view have been so far completely lacking, and are proposed with the present study. Symptomatic depressive conditions in diabetes are frequent and should be primarily separated from depressive endogenous psychosis. The pathogenesis of the association between diabetes of the adult-obese type and psychosis might be discussed according to a transactional theoretical model, assuming a positive feed-back mechanism of the two relationships: diabetes-psychosis and psychosis-diabetes. With these criteria, 4 observations of the clinical association were collected out of 274 admissions for diabetes, during 1976. Diabetes is intended as overt diabetes; obesity presented with the stenic picture; psychosis had a monopolar melancholic course. Similar clinical features were characteristic in all cases. The relationship diabetes-psychosis showed no evidence, unless importance should be given to a potential diabetes in 3 cases. On the contrary, the relationship psychosis-diabetes could be demonstrated in the four cases. A psychosomatic scheme connecting the neuro-hormonal correlations to a genetically conditioned exhaustion of the beta-function, is postulated. During melancholic recurrences, diabetes proved to be insulin-dependent and even insulin-resistent in 2 cases. Tricyclic antidepressant theraphy did not modify the metabolic situation.
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PMID:[Association of adult obese-type diabetes and depressive psychosis (clinical cases)]. 61

Mammals and birds adapt to prolonged fasting by mobilizing fat stores and minimizing protein loss. This strategy ends with an increase in protein utilization associated with behavioural changes promoting food foraging. Using the Zucker rat as a model, we have investigated the effect of severe obesity on this pattern of protein loss during long-term fasting. Two interactions between the initial adiposity and protein utilization were found. First, protein conservation was more effective in obese than in lean rats: fatty rats had a three times lower daily nitrogen excretion and proportion of energy expenditure deriving from proteins, and a lower daily protein loss in various muscles. This phase of protein sparing is moreover nine times longer in the fatty rats. Second, obese animals did not show the late increase in nitrogen excretion that occurred in their lean littermates. Total body protein loss during starvation was larger in fatty rats (57% versus 29%) and, accordingly, total protein loss was greater in their muscles. At the end of the experiment, lean and obese rats had lost 98% and 82%, respectively, of their initial lipid reserves, and fatty rats still had an obese body composition. These results support the hypothesis that in severely obese humans and animals a lethal cumulative protein loss is reached long before the exhaustion of fat stores, while the phase of protein conservation is still continuing. In contrast, in lean rats, survival of fasting seems to depend on the availability of lipid fuels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationships between lipid availability and protein utilization during prolonged fasting. 150 87

Eleven obese patients, 5 males; age: 17-42; body mass index (BMI): 40; % of ideal weight: 187%, and 10 normal subjects (5 males; age: 19-39; BMI: 22; % of ideal weight: 103%), both groups without heart and respiratory disorders, underwent a cycloergometric test with subsequent 20-watt increases every 4 min until exhaustion. During the test, ventilation/minute, expiratory gas concentration and heart rate were measured, and the anaerobic threshold (AT) was determined in each subject. The obese patients showed a significantly lower AT than normal subjects (p less than 0.01); showing values which decreased with the increase in the grade of obesity expressed in BMI or in percent of their ideal weight. Moreover, in the obese patients, the O2 consumption (VO2) had significantly increased compared to that of normal subjects at no resistance and at all work levels. The negative correlation between the AT value and the BMI in obese patients can attribute their increase in VO2 during stress to (1) the inertial overloading caused by obesity especially considering the adipose tissue of their legs, or (2) to their level of 'fitness' being lower than that of normal subjects.
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PMID:Relationship between body mass and tolerance to physical stress in obese patients. 179 23

Most incidence studies indicate that baseline plasma glucose, either fasting or post-glucose load, is the best predictor of progression to non-insulin-dependent diabetes mellitus (NIDDM)--the higher the level, the higher the risk. Elevated serum insulin concentrations in the presence of normal fasting plasma glucose levels reflect the presence of insulin resistance and they have also been shown to predict deterioration to NIDDM in a number of populations. Hyperinsulinaemia is a notable characteristic of populations with a high prevalence of NIDDM such as Micronesian Nauruans, American Pima Indians, Mexican-Americans and Asian Indians. In Nauruans and Pima subjects with normal glucose tolerance, those with higher post-load (2-hour) serum insulin at baseline were more likely to progress to either impaired glucose tolerance (IGT) or NIDDM. Conversely, amongst subjects with IGT, progression to NIDDM was predicted by lower (but still high relative to normal) baseline insulin responsiveness. Similar results for subjects with IGT have been described in Japanese. It appears from longitudinal studies that baseline insulin and glucose levels explain much of the association of obesity with risk of NIDDM. It remains to be resolved whether obesity itself may be a manifestation of an underlying defect (such as primary hyperinsulinaemia) which leads to both obesity and NIDDM. The possible sequence of events for the development of NIDDM includes a genetic defect resulting in hyperinsulinaemia and/or insulin resistance and leading ultimately to secondary pancreatic exhaustion with an insulin secretory defect which may also be genetically determined or the result of glucotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperinsulinaemia is a predictor of non-insulin-dependent diabetes mellitus. 193 64

Clinical and physiological data on long-term follow-up of 143 patients with respiratory-dependent pacemakers (RDP3) are reported; 121 patients received ventricular (VVI-RD) and 22 patients atrial (AAI-RD) respiratory-dependent stimulation. Functional evaluation was based on the exercise testing (130 pts) with oxygen uptake VO2, ventilation, ECG and arterial pressure monitoring and the dynamic Holter electrocardiogram (95 pts). In each patient, the stimulation rate curve selected was that which produced the best work tolerance and moved the anaerobic threshold to the right. Respiratory levels were assessed by telemetry verifying proper sensing of tidal volume variations and absence of interference and artefacts. In patients with VVIR or AAIR stimulation, exercise tolerance, oxygen uptake and anaerobic threshold increased significantly in comparison with VVI or AAI pacing respectively. The physiological sensitivity of the stimulation system (i.e., a linear relationship of the pacing rate with metabolic requirements) was excellent (up to exhaustion) in 70%, very good (up to anaerobic threshold) in 20% and erratic (no relationship between pacing rate and VE/VO2) in 10% of patients. In dynamic electrocardiographic monitoring, the automatic pacing rate was always predominant during the night and during rest periods; the pacing rate increased properly with daily activity; myopotential inhibition (none longer than 3,500 ms) was observed in 38 patients, but without subjective complaints. The incidence of the RDP3 malfunction was less than 8%; it may have stemmed from the pacing system itself, or from other clinical conditions. Oversensing of impedance system pulses has not been recorded in the last 3 years. Partial respiration undersensing results from incorrect accessory lead position, pulmonary emphysema, marked obesity or other causes. Respiratory sensing becomes erratic at the anaerobic threshold point in such patients, but functions well at submaximum exercise levels. In patients with left ventricular failure, exercise tolerance was improved by setting a lower ratio between the pacing rate and respiration, which prevented the occurrence of excessive pacing rates.
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PMID:Physiological sensitivity of respiratory-dependent cardiac pacing: four-year follow-up. 246 Aug 30

Sustained elevations of plasma glucose and insulin concentrations follow intense (80% maximum oxygen uptake) exercise performed in the postabsorptive state. To provide insights into possible mechanisms and influence of obesity, 8 lean and 12 obese subjects [106 +/- 11% (SD) and 193 +/- 31% of reference table weight, respectively] eating previously isocaloric diets were exercised to exhaustion (7 +/- 3 min) on a cycle ergometer, then followed for 60 min of recovery. The obese subjects at rest had slightly increased plasma glucose and insulin and elevated blood glycerol concentrations. Both lean and obese subjects had little or no changes in plasma glucose or insulin during exercise, but the increases during the recovery period were greater and/or sustained longer in the obese. Such results raise the possibility of transient hepatic insulin resistance after exercise and are possibly relevant to restoration of depleted muscle glycogen. Both groups had a marked fall in plasma FFA during exercise; the reduction was sustained in the lean but not in the obese subjects. Blood glycerol increased during the recovery period to higher values in the obese than in the lean subjects. Plasma norepinephrine increased about 4-fold in both groups, returning promptly to preexercise values. In contrast, the exercise-induced increment in plasma epinephrine [values at exhaustion, 933 +/- 548 vs. 1970 +/- 787 pmol/L; P less than 0.005] was markedly attenuated in the obese subjects. Thus, the obese subjects had exercise-induced changes in glucose and inulin metabolism consistent with greater postexercise insulin resistance, despite an impaired plasma epinephrine response to intense exercise.
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PMID:Metabolic responses to intense exercise in lean and obese subjects. 264 9

Sixty-seven subjects with moderate obesity (50 +/- 3 percent above ideal body weight) were given an oral glucose tolerance test with the simultaneous measurement of rates of glucose and lipid oxidation by continuous indirect calorimetry. When the subjects were stratified into nine 5-year classes of duration of obesity, the prevalence of impaired glucose tolerance (IGT) and overt diabetes both increased with increasing duration of obesity. Both basal and post-OGTT lipid oxidation rates were, however, similar in all classes. To assess the independent influence of IGT, diabetes, age, and duration of obesity on glucose metabolism, the data were subjected to analysis of variance using a factorial design with metric covariates. Age by itself was found to be associated (P less than 0.05) with a decline in total post-OGTT glucose oxidation. Both IGT and diabetes, on the other hand, were associated with increased plasma insulin and free fatty acid (FFA) levels, both in the fasting state and following glucose ingestion (P = 0.05-P less than 0.002). Only diabetes, however, was associated with a drastic reduction in nonoxidative glucose disposal, which marked the appearance of, and strongly correlated with (r = -0.81, P less than 0.001), fasting hyperglycemia. Duration of obesity had significant metabolic consequences in its own right: a fall in the insulin response to glucose (P = 0.05) and in the rate of total glucose oxidation (P = 0.03), and a rise in post-OGTT glucose levels (P = 0.04). We conclude that: (a) increased lipid oxidation is common in obesity, but is not sufficient to explain the deterioration of glucose tolerance in long-term obesity; (b) very-long-term obesity may be associated with partial exhaustion of the beta cell, and the resultant insulinopenia may cause depressed glucose oxidation and impaired glucose tolerance, and (c) a defect in nonoxidative glucose disposal is a characteristic feature of frank diabetes at any stage of obesity.
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PMID:The metabolic consequences of long-term human obesity. 306 64

Via the artificial endocrine pancreas--apparatus "BIOSTATOR" 100 patients were studied and treated, namely: 90 with diabetes mellitus, 7 with hyperinsulinism and 3 with obesity. The 24-h insulin needs of the diabetics with insulin-dependent and non-insulin dependent with secondary exhaustion type of diabetes, were determined. The following subcutaneous insulin dosage was determined, depending on the insulin amount spent during the 24-h biostator control. It was established that the necessary reduction of the intravenously administered insulin is 30% on the average with the passing over to subcutaneous regime. The indices of lipid metabolism were also studied as well as numerous hormones with which the carbohydrate compensation leads to a change. The problem of the "morning" phenomenon is discussed.
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PMID:[Use of the artificial endocrine pancreas in the clinic]. 409 82


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