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Biomedical subjects
Publications and source records attributed to R Sörbris.
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Fifteen grossly obese patients were studied before and 6-8 months after gastroplasty. Their mean body weight decreased by 30% (from 127 +/- 13 to 97 +/- 14 kg, mean +/- SD). The preoperative hyperinsulinemia, hyperglucosemia and hyperglucagonemia were significantly reduced at follow up. Liproprotein lipase activity, measured in post-heparin plasma, was slightly reduced and did not change after weight reduction. Variables reflecting thyroid function were within the reference ranges; small but statistically significant reductions in serum thyroxine and reverse triiodothyronine levels were recorded. Adipocyte heat production, reflecting total cellular metabolic activity and registered by microcalorimetry, was significantly decreased before surgery (by about 60 per cent when expressed per g tissue and by about 20 per cent when expressed per cell) and increased significantly at follow-up; expressed per cell, the heat production was normalized, but expressed per g tissue the values were still about 15 per cent before those of a control group. The results indicate that the reduced adipocyte heat production in obese individuals is a consequent rather than a cause of severe obesity.
Twenty-four grossly obese patients were operated on with horizontal gastroplasty. One patient died postoperatively of pulmonary embolism. The remaining 23 were extensively studied before and repeatedly after surgery. Eighteen months postoperatively the average weight loss was 34.4 kg (range, 1-71 kg). Seven patients had a weight reduction of less than 20% after 18 months. Postoperatively, biochemical variables reflecting glucose and lipid metabolism and liver function improved. B-hemoglobin, S-iron levels, and serum concentrations of folate and cobalamins decreased significantly. No negative histological changes could be found in the gastric mucosa during the follow-up period. Although only positive metabolic changes have been registered, we feel that gastroplasty, which is not without early postoperative complications and has a failure rate of about 30%, cannot be generally recommended until the problem of postoperative dilation of the stoma has been successfully solved.
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We have studied effects of weight reduction after gastroplasty on glucose and lipid metabolism in 15 grossly obese subjects. Their body weight decreased from 127 +/- 13 to 97 +/- 14 kg 6 months after surgery and remained essentially stable 8 months later. There was a marked improvement of lipid and carbohydrate metabolism with significant reductions in blood glucose, plasma insulin and glucagon levels, and in glucose tolerance. Lipoprotein lipase activity in adipose tissue was in the upper reference range and lipoprotein lipase activity in postheparin plasma tended to be low. Plasma triglyceride, cholesterol and low-density lipoprotein cholesterol concentrations decreased significantly, while high-density lipoprotein cholesterol levels tended to rise. Concomitantly, there was an increase in triglyceride clearance rate. Most of these changes were significantly correlated to the reduction in body weight/body fat, indicating that the metabolic improvements are due to body fat reduction as such.
A reduction in the number of postoperative bed days for patients who underwent appendectomy led to a study of changes in hospital costs of appendectomies for the years 1955, and 1965, and 1975. No significant changes were found in the total hospital costs. However, the postoperative costs decreased by 36 percent from 1955 to 1975 due to a decrease in the mean duration of hospital stay. During the same period of time, the perioperative costs increased by (table; see text) 90 percent due to increased length of operation time correlated with an increasing proportion of inexperienced operating surgeons. At present, there seem to be few possible ways to increase the cost efficiency of treating appendicitis.
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Microcalorimetry has been employed to measure the heat production by adipocytes obtained by percutaneous biopsy from lean subjects and from obese subjects before and after weight reduction. Cellular heat production was significantly lower in obese than in lean subjects. After weight reduction cellular heat production increased in fat cells from the obese subjects but was still significantly lower than in cells from control subjects. A number of variables reflecting uptake and mobilization of depot fat have measured and correlated to the heat production values in the obese subjects. The findings are consistent with the view that a decreased total metabolic activity might contribute to the development or perpetuation of obesity.
The effects of vegetarian fasting were evaluated in 14 grossly obese patients who participated in a program comprising 5 weeks' fasting in a lactovegetarian health center. Before and after the fasting period the patients were hospitalized and put on a standardized weight-maintaining diet; at the health center they consumed vegetable juices containing less than 1 MJ and 3 g of protein per day. The weight reduction (mean +/- S.D.) was 13.4 +/- 5.0 kg (from 132.0 +/- 27.2 to 118.6 +/- 16.1 kg). Except for the first few days the patients had no severe hunger sensations. No severe adverse clinical effects were noted. The laboratory status--comprising serum or plasma levels of minerals, protein, and lipids; hematological data; and variables reflecting liver and thyroid function--revealed abnormal group mean values only for ferritin and the acute-phase reactants haptoglobin, C-reactive protein, and anti-chymotrypsin in the obese. The levels of potassium, retinol-binding protein, and haptoglobin decreased, and aminotransferase and lactate dehydrogenase activities and free fatty acid and glycerol concentrations increased as a result of the fasting. The most striking effect of the weight reduction was an increase in the HDL cholesterol levels. Fasting according to the described regimen thus seems to provide a safe method for treatment of obese patients.
The effect of five weeks fasting on body weight, lean body mass and fat weight was studied in 14 obese subjects (BW 92-200 kg, Broca's index 1.3-2.4). Before and after treatment the patients were hospitalized and put on a standardized weight maintaining diet, and variables reflecting thyroid function were compared before and after weight reduction. There was a considerable variability in the reduction of body weight (4-22 kg), lean body mass (1-7 kg) and fat weight (4-18 kg). None of the thyroid variables were correlated to the degree of obesity. The body weight loss during treatment was correlated to initial body weight, initial lean body mass and initial body fat weight. The reduction in body fat, however, was significantly correlated only to initial body weight (r=0.70) and lean body mass (r=0.61). Plasma concentrations of thyroxine, triiodothyronine and reverse triiodothyronine were not related to reduction of body fat, whereas the T3 uptake test was significantly correlated to the fat weight loss (r = 0.67). Multiple regression analyses demonstrated in the initial body weight and T3 uptake were independently correlated to fat weight reduction. Together these variables accounted for about 75 per cent of the variability in fat weight reduction during fasting therapy. Plasma concentrations of rT3 before treatment was significantly correlated to the reduction lean body mass (r=0.78), whereas rT3 was not related to fat weight reduction (r=0.28). The determination of thyroid hormones and T3 uptake seems to have prognostic value for the effect of caloric restriction on different metabolic compartments.
The relationship between obesity and alterations in adipose tissue metabolism and lipid transport was studied in fourteen obese subjects before and after a weight reduction of 4-22 kg. Blood glucose and plasma insulin patterns after peroral glucose intake improved significantly, and plasma glucagon levels decreased markedly after treatment. Plasma triglyceride and total cholesterol levels were not altered, but there was a 20% (P less than 0.05) increase in HDL concentrations. Plasma free fatty acid and glycerol concentrations decreased, in parallel to a decrease in lipolysis rate in vitro. Lipoprotein lipase and hepatic lipase activities in postheparin plasma, as well as the intravenous fat tolerance test, were normal and did not change significantly after weight loss. Lipoprotein lipase activity in adipose tissue, expressed per cell, was elevated and did not change after weight reduction. Also, the enzyme activity did not increase after glucose intake before or after treatment. The lack of effect on lipoprotein lipase activity and regulation in combination with significant improvements of other aspects of lipid and glucose transport is consistent with the view that alterations in LPL activity and regulation may represent an early and possibly primary defect in the development of obesity.
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A method for the quantitative measurement of heat production in isolated human adipocytes is described. Fat cells are isolated by collagenase treatment of biopsy specimens of adipose tissue, and heat production measured by microcalorimetry. The heat effect was constant for at least 4 h. Heat values increased with increasing pH (about 6% per 0.1 pH unit) and temperature (about 9% per degrees C at 37 degrees C). The apparent activation energy was calculated as 44 kJ/mol. Heat production was about 50% higher in cell suspensions containing glucose and insulin. Imprecision was about 6.5% (coefficient of variation) and sensitivity allowed measurements in samples containing 20-30 mg adipocyte lipid. Heat production in normal volunteers under standardized conditions (i.e. in Krebs-Ringer-bicarbonate buffer pH 7.4, at 37 degrees C and in the presence of 11 mmol/l glucose and 0.1 U/ml insulin) was 133 +/- 48 (mean +/- SD) microW/g adipocyte lipid weight, corresponding to 49 +/- 15 pW/cell. The technique seems of importance for the characterization of energy balance in the fat cell under normal and pathophysiological conditions.
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The costs for elective cholecystectomies were measured 1955, 1965 and 1975. The average length of stay decreased by 25% between 1955 and 1965 and with the same amount between 1965 and 1975. In spite of these marked reductions in the average length of stay there was only a significant decrease in costs between 1955 and 1965 but not between 1965 and 1975.
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