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Biomedical subjects

B Richelsen

Publications and source records attributed to B Richelsen.

At least 73 records · Page 4Linked to original sources
PubMed1995

Associations between different anthropometric measurements of fatness and metabolic risk parameters in non-obese, healthy, middle-aged men.

OBJECTIVE: To investigate whether body fatness influences the metabolic risk profile in a group of healthy, normal-weighted men and to determine which anthropometric measurements that are most closely associated with the risk profile in this group of men. DESIGN: A cross-sectional study where total fatness and abdominal fatness were determined by older (BMI, WHR, impedance) and more recent anthropometric indices (sagittal diameter (SD) and conicity index (Valdez et al., Int. J. Obes. 1993; 17: 955)). The metabolic risk profile was determined by lipoproteins, insulin, glucose and blood pressure. SUBJECTS: The study comprised a homogeneous group of 58 men who were all healthy and normal-weighted (BMI = 24.2 +/- 1.8) and were all 44 years old. RESULTS: In relation to total fatness, BMI was more closely correlated to the various risk parameters than the fat mass determined by bioelectrical impedance independent of using several different equations in estimating the fat mass. From simple comparison of correlation coefficients, SD and SDH (SD/height) seemed to be the best indices of abdominal fatness in predicting an enhanced metabolic risk profile. The conicity index was considerably inferior in comparison to the other indices of abdominal fatness. In multiple regression analysis abdominal fatness as determined by SD or SDH explained most of the variation in the metabolic risk profile and no significant influence of total fatness (BMI) was found when taking the influence of abdominal fatness into account. The most pronounced effect of abdominal fatness in these non-obese men was a reduction of HDL-cholesterol, an elevation of the triglycerid level and an elevation of the insulin level. CONCLUSION: Thus, even a minor accumulation of adipose tissue in the abdominal region in these otherwise non-obese men was associated with a considerably adverse metabolic risk profile. SD or SDH seemed to be slightly more correlated to the risk profile than other anthropometric indices of abdominal adipose tissue mass (e.g. WHR). The new conicity index was inappropriate for predicting the risk profile associated with abdominal fatness in these non-obese men.

Abdomen↗
PubMed1994

[The importance of nutrition for the prevention of osteoporosis].

The prevalence of osteoporosis is increasing, and is a significant burden on society. Dietary composition is an important determinant of the bone mineral density in the growth period, and of the magnitude of the age related bone mineral loss, in particular among postmenopausal women. Therefore, an improvement of the diet has an important role in the prevention of osteoporosis. A sufficient intake of calcium and vitamin D can reduce the risk of fractures in postmenopausal women, and it is likely that a low calcium intake may affect peak bone mass negatively. Calcium in the Danish diet comes mainly from dairy products. Half a litre of milk and 25 g of cheese will cover most people's calcium requirement. Part of the calcium requirement may also be covered by consuming other foods such as cabbage, broccoli and beans. Children, adolescents and elderly individuals who avoid dairy products are recommended to take a calcium supplement. The status of vitamin D among the elderly can be improved by a daily outdoor stay and by a frequent intake of fatty fish such as herrings. Elderly persons who stay indoors are recommended to take a vitamin D supplement.

Adolescent↗
PubMed1994

Augmented effect of short-term pulsatile versus continuous insulin delivery on lipid metabolism but similar effect on whole-body glucose metabolism in obese subjects.

The present study was designed to examine the effect of pulsatile versus continuous insulin delivery on glucose and lipid metabolism in insulin-resistant subjects. Six obese women (body mass index, 40.0 +/- 2.8 kg/m2) underwent a euglycemic glucose clamp (plasma glucose, 90 mg/dL) twice. In random order, insulin was infused intravenously for 375 minutes either at a constant rate (0.4 mU/kg/min) or in a pulsatile manner (2.4 mU/kg/min for 2 minutes followed by an off interval of 10 minutes). Endogenous insulin release was suppressed by infusion of somatostatin (250 micrograms/h). Mean circulating insulin concentrations were similar during the two protocols (pulsatile v continuous infusion, 60 +/- 10 v 56 +/- 9 mU/L), but pulsatile infusion was accompanied by oscillations with an amplitude of 120 mU/L. After 6 hours of pulsatile versus continuous insulin, isotopically determined total glucose disposal (3-3H-glucose) and hepatic glucose production (HGP) were comparable (pulsatile v continuous, 2.80 +/- 0.56 v 2.82 +/- 0.51 and 0.37 +/- 0.14 v 0.32 +/- 0.17 mg/kg/min). However, the rate of glucose oxidation (indirect calorimetry) was augmented (P < .05), whereas lipid oxidation tended to be diminished (.10 > P > .05) following pulsatile infusion. In addition, blood glycerol was more suppressed with pulsatile (31 +/- 9 nmol/L) than with continuous infusion (36 +/- 10 nmol/L, P < .05), whereas blood lactate, alanine, and 3-hydroxybutyrate were similar in the two infusion protocols.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Fuel metabolism, energy expenditure, and thyroid function in growth hormone-treated obese women: a double-blind placebo-controlled study.

Growth hormone (GH) promotes protein anabolism and lipolysis. Its effects on glucose metabolism include suppression of glucose oxidation and may be associated with insulin resistance. In addition, GH stimulates energy expenditure (EE) and peripheral thyroid hormone metabolism. GH secretion is reduced in obese patients, but whether this is of pathophysiological significance is incompletely understood. In a double-blind placebo-controlled crossover design, we studied the effects of GH administration (0.03 mg.kg ideal body weight [IBW]-1.d-1) on fuel metabolism, EE, and thyroid function in 10 obese women (age, 30.4 +/- 2.4 years; body mass index [BMI], 37.0 +/- 2.8 kg/m2, mean +/- SE) with a normal prestudy oral glucose tolerance test (OGTT). Each treatment period (GH or placebo) lasted 5 weeks, separated by a 5-week washout period. At the end of each treatment period, subjects were studied in the basal state (8:00 AM) and during a euglycemic glucose clamp including indirect calorimetry and isotopic measurement of glucose turnover. Lean body mass (LBM) was assessed at the end of each period by dual-energy x-ray absorptiometry. In the basal state, GH induced a significant increase in circulating levels of free fatty acids (FFA), glucose, insulin, and C-peptide. This was associated with a significant increase in resting EE (kcal/24 h, 1,934 +/- 92 placebo v 2,323 +/- 134 GH, P < .001), a decrease in the respiratory exchange ratio (RER), and increased rates of lipid oxidation (mg.kg LBM-1.min-1, 1.55 +/- 0.09 placebo v 2.20 +/- 0.13 GH, P < .01). GH increased the rate of total basal glucose turnover, whereas oxidative glucose disposal was significantly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Growth hormone treatment of obese women for 5 wk: effect on body composition and adipose tissue LPL activity.

Because it has been found that growth hormone (GH) treatment of GH-deficient adults is able to reduce the total fat mass, the present study was undertaken to investigate the effect of GH treatment in obese subjects. The investigation was a double-blind placebo-controlled crossover study in which nine obese females were treated with GH (0.03 mg.kg ideal body wt-1.day-1) and placebo for 5 wk. Body composition was determined by dual-energy X-ray absorptiometry, and the quantity of intra-abdominal adipose tissue was determined by CT scan. Lipoprotein lipase (LPL) activity was determined in fat biopsies taken from the subcutaneous abdominal and gluteal region. GH treatment significantly reduced the total fat mass from 40.5 to 38.4 kg (i.e., 5% reduction of the total fat mass; P < 0.01), whereas the fat-free mass increased from 50.5 to 53.5 kg (P < 0.01). In addition, GH treatment significantly reduced the intra-abdominal adipose tissue determined by CT scan (reduction by 7 +/- 0.3%; P < 0.02). CT scan performed at the level of the femur showed a 7% reduction in adipose tissue and a 5% increase in muscle volume in the GH group (P < 0.05). Thus no clear regional differences in the GH-mediated reduction of the adipose tissue mass were observed. GH reduced the LPL activity by approximately 50% (P < 0.01) in the adipose tissue. Finally, GH treatment significantly increased the level of plasma free fatty acids (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Characterization of regional and gender differences in glucocorticoid receptors and lipoprotein lipase activity in human adipose tissue.

Glucocorticoid receptor (GR) status was studied in adipose tissue from omental and sc abdominal adipose tissue. As the effects of glucocorticoids may be due to alteration of triglyceride uptake in adipose tissue, the activity of the enzyme lipoprotein lipase (LPL) was also investigated. Fat biopsies were obtained from 8 women and 11 men matched for age and body mass index. Omental adipose tissue contained 4 times the number of GR as sc abdominal adipose tissue (42.0 +/- 4.1 vs. 10.5 +/- 2.3 fmol/mg protein, respectively; P < 0.001) with similar Kd values. No gender difference in GR number was observed in adipose tissue from the two regions. LPL activity in omental adipose tissue was about 820 nmol FFA/h.g wet wt in both sexes, whereas LPL activity in sc adipose tissue was about 2- to 4-fold lower. Moreover, LPL activity in sc adipose showed marked gender differences, with 2-fold higher activity in women than in men (474 +/- 84 vs. 238 +/- 35 nmol FFA/h.g wet weight; P < 0.03). Finally, there was no correlation between GR number and LPL activity when each fat depot was investigated separately. However, a positive correlation between LPL activity and glucocorticoid binding was found when the data from both regions were pooled (r = 0.55; P < 0.01). In conclusion, human adipose tissue dexamethasone binding was higher in omental than in sc adipose tissue, without any gender difference. LPL activity was also higher in omental than in sc adipose tissue in both groups, without any gender difference. On the other hand, sc LPL activity was higher in females than in men. A correlation (positive) between GR number and LPL activity was only found when the data from both regions were pooled.

Adipose Tissue↗
PubMed1993

[Cholesterol-lowering effect of a new fermented milk product in healthy 44-year old Danish men].

The potential cholesterol-lowering effect of a new fermented milk product was tested in a homogeneous group of Danish men (all 44-year-old; n = 58) in a randomised, double blinded and placebo-controlled study. Two hundred ml of the fremented milk or placebo (chemically acidified) was taken daily for six weeks. After these six weeks total cholesterol decreased significantly in the fermented milk group by -0.37 mmol/l (confidence interval: -0.51 to -0.23 mmol/l) and no changes were observed in the placebo group (-0.02 mmol/l) (p < 0.01). This decrement in total cholesterol could be completely ascribed to a reduction of LDL-cholesterol by 10% (i.e. -0.42 mmol/l), since HDL-cholesterol and triglyceride were unchanged in both groups during the study. Thus, in the present short term study, the tested fermented milk product was able to reduce LDL-cholesterol in middle-aged men.

Adult↗
PubMed1993

Abdominal obesity is associated with insulin resistance and reduced glycogen synthetase activity in skeletal muscle.

Insulin resistance is commonly associated with obesity. The present study was performed to investigate the relative importance of total fat mass versus localization of adipose tissue in insulin-stimulated glucose disposal (Rd) and skeletal muscle glycogen synthase (GS) activity in obese individuals. Twenty obese women with an average body mass index (BMI) of 37.8 +/- 1.3 kg/m2 and a waist to hip ratio (WHR) ranging from 0.78 to 1.02 were examined during basal conditions and following hyperinsulinemia (hyperinsulinemic euglycemic clamp). To accurately determine body composition, the following three methods were used: anthropometric measurements, dual-energy x-ray absorptiometry scanning (DEXA-scan), and bioelectric impedance measurements. In addition, indirect calorimetry and muscle biopsy were performed. Insulin-stimulated glucose Rd was negatively correlated with WHR (R = -.52, P < .025) whereas there were no correlations with BMI or percent fat (R = .16, NS and R = .16, NS, respectively). Furthermore, a negative correlation between WHR and insulin stimulation of GS activity in skeletal muscle was found (R = -.62, P < .005). In contrast, BMI and percent fat were not correlated with the insulin effect on GS activity in skeletal muscle (R = .34, NS and R = -.35, NS, respectively). The concentration of nonesterified fatty acids (NEFA) during hyperinsulinemia was strongly correlated with WHR and abdominal localization of adipose tissue (determined by DEXA-scan; R = .60, P < .005 and R = .60, P < .007, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1993

Lipoprotein lipase activity in muscle tissue influenced by fatness, fat distribution and insulin in obese females.

Obesity is associated with dyslipidaemia and increased morbidity and mortality from premature atherosclerosis and diabetes mellitus. Particularly, hypertriglyceridaemia is a characteristic finding in patients with obesity. In addition, the elevated levels of triglycerides may be an important risk factor for development of the obesity-related complications. Lipoprotein lipase activity in skeletal muscle tissue (mLPL) has previously been found to be an important factor regulating the concentration of serum triglycerides. To describe the relationship between mLPL, triglycerides and fatness/fat distribution in more detail we have investigated these parameters under basal conditions and during insulin stimulation in 20 obese females. During hyperinsulinaemia (204 microU ml-1) for 4 h the mLPL activity decreased from 528 +/- 52 nmol FFA g-1 to 412 +/- 44 (P < 0.001). Basal mLPL was negatively correlated with serum triglycerides (r = -0.48, P < 0.05) and positively correlated with HDL-cholesterol (r = 0.58, P < 0.01). Employing multiple variance analysis it was found that both BMI and WHR were negatively correlated to mLPL, however, the impaired lipid profile (high triglyceride, low HDL-cholesterol, high FFA) could only be related to BMI and not to WHR in these obese females. However, reduced insulin-action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin-effect on mLPL as well as for the insulin-effect on whole-body glucose metabolism (clamp-study).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1993

Inhibition of renal ornithine decarboxylase activity prevents kidney hypertrophy in experimental diabetes.

The selective ornithine decarboxylase (ODC) inhibitor difluoromethyl ornithine (DFMO) was used to investigate the role of polyamines in initial diabetic renal enlargement. ODC activity in kidneys from diabetic animals was increased (fivefold) 24 h after diabetes induction (P < 0.05), and throughout the study (7 days) the activity remained 2- to 3-fold elevated (P < 0.05). Insulin treatment normalized renal ODC activity, whereas DFMO treatment totally inhibited the kidney ODC activity. The kidney weight in diabetic rats was 21% higher than that of control rats (1,074 +/- 35 mg and 889 +/- 16 mg, P < 0.001). Insulin treatment normalized kidney weight (847 +/- 13 mg). Despite unaltered diabetic metabolic aberrations the kidney weight in DFMO-treated diabetic rats was normalized (911 +/- 7 mg). In conclusion, the ODC activity in diabetic kidneys undergoing hypertrophy was increased. Insulin treatment normalized both kidney weight and kidney ODC activity. Finally, selective inhibition of ODC activity by DFMO resulted in kidneys of normal size, despite unaltered diabetic metabolic aberrations. These findings support the hypothesis that polyamines play an important role in initial diabetic renal enlargement.

Animals↗
PubMed1993

Influence of short-term dexfenfluramine therapy on glucose and lipid metabolism in obese non-diabetic patients.

In a short-term (eight days) double-blind crossover study involving 10 obese patients, the effects of dexfenfluramine on glucose and lipid metabolism were examined. The protocol comprised whole body in vivo measurements (hyperinsulinemic euglycemic clamp in combination with indirect calorimetry) and in vitro studies of isolated adipocytes (lipolysis and glucose transport). All study participants were weight stable during the study period (103.1 +/- 3.2, placebo vs 103.3 +/- 3.1 kg, dexfenfluramine, NS). The following parameters were significantly reduced after dexfenfluramine treatment: fasting levels of plasma glucose (6.2 +/- 0.2 vs 5.7 +/- 0.2 mmol/l, p < 0.01), serum insulin (168.0 +/- 14.5 vs 138.9 +/- 7.9 pmol/l, p < 0.05), serum C-peptide (0.68 +/- 0.03 vs 0.58 +/- 0.02 nmol/l, p < 0.05) and total serum cholesterol (6.07 +/- 0.41 vs 5.48 +/- 0.38 mmol/l, p < 0.01). In the basal state glucose oxidation rate was significantly reduced by 36% (p < 0.001), whereas non-oxidative glucose disposal was significantly increased by 41% (p < 0.01), following dexfenfluramine treatment. Insulin-stimulated (2 mU.kg-1 x min-1) glucose disposal rate tended to be increased (18%, p = 0.10) after dexfenfluramine. In conclusion, dexfenfluramine possesses beneficial regulatory effects on glucose and lipid metabolism in non-diabetic obese patients, independently of weight loss.

Adipose Tissue↗
PubMed1992

[Over-the-counter weight-reducing preparations].

This report deals with over-the-counter products sold currently in Denmark for weight reduction. Only oral products (alternative medications and food supplements) are included. The report includes 35 such products. The aims of the report are to provide a common, factual basis for the debate about weight-reduction products and to present proposals for regulations that improve the conditions for patients and health professionals to make their choice of the optimal products. Current laws and administrative regulations are found to be complicated, obscure and inadequate. For most products, documentation for efficacy and safety is inadequate and health hazards are probable using several of the products. It is recommended 1) that obesity should be considered as a disease also in a legal/administrative context, 2) that an effective and objective registration of side-effects to alternative medication and food supplements is established, 3) that these products are tested for efficacy and safety before being marketed, 4) that the entire product information is made easily accessible, 5) that products without any documented effect are clearly labelled with this information and 6) that weight loss products involving health hazards are excluded from the market.

Denmark↗
PubMed1992

Characterization of nuclear corticosteroid receptors in rat adipocytes. Regional variations and modulatory effects of hormones.

The corticosteroid receptor was investigated in isolated rat adipocytes with a new technique which characterizes the corticosteroid receptors that can be activated and tightly bound to the nucleus. The binding reaction with [3H]triamcinolone was performed with intact isolated adipocytes and the radioactivity associated with nucleus was subsequently determined after cell lysis. Scatchard analysis revealed a homogeneous class of nuclear corticosteroid receptors in rat epididymal adipocytes with an apparent Kd of 4.93 +/- 1.5 nM and a Bmax of 21.8 +/- 6.6 fmol/10(6) cells corresponding to about 13,000 receptors per nucleus. The corticosteroid binding exhibited regional variations in isolated adipocytes. The highest receptor number was found in epididymal adipocytes (Bmax 25.8 +/- 3.9 fmol/10(6) cells) whereas there were significantly lower nuclear binding sites in perirenal adipocytes (16.5 +/- 5.5 fmol/10(6) cells) (P less than 0.05) and subcutaneous adipocytes (4.8 +/- 1.5 fmol/10(6) cells) (P less than 0.01). The apparent affinity in the three fat depots were similar with Kd values about 4 nM. The nuclear corticosteroid receptor in adipocytes was steroid specific, as neither unlabelled estradiol nor testosterone were able to displace the [3H]triamcinolone binding at concentrations up to 100 microM. However, unlabelled progesterone and promegestrone (R5020) were able to compete with triamcinolone-binding (by 50-80%). In order to investigate whether the nuclear corticosteroid binding in adipocytes were under influence of other hormones we examined the effects of lipolytic and antilipolytic compounds on the binding. Preincubation with isoproterenol and dibutryl-cAMP for 1 h was able to decrease the corticosteroid binding by 30-50%. However, the antilipolytic hormone insulin had no effect in preincubations performed for up to 2 h. In conclusion, high affinity nuclear corticosteroid receptors were found in rat adipocytes. These receptors exhibited regional variations and were modulated by lipolytic hormones.

Adipose Tissue↗
PubMed1992

Effects of in vivo estrogen treatment on adipose tissue metabolism and nuclear estrogen receptor binding in isolated rat adipocytes.

We have previously demonstrated the existence of nuclear estrogen receptors in isolated adipocytes (Pedersen et al. (1991) Biochim. Biophys. Acta 1093, 80-86). In the present study we have investigated the regulatory properties of these nuclear estrogen receptors, in addition to the metabolic effects of estrogen on adipose tissue metabolism. Estrogen treatment (20 micrograms 17 beta-estradiol in NaCl for 7 days) decreased lipoprotein lipase activity (LPL) in the adipose tissue by 62% (p less than 0.05), decreased adipocyte size by 27% (p less than 0.01) and diminished the normal postovariectomy weight gain. Furthermore, estrogen treatment increased the nuclear estrogen receptor binding in adipocytes; in addition, there was a tendency for increased cytosolic estrogen receptor content as well. Time course studies revealed that already 6 h after a single estrogen injection the Bmax increased from 3.82 +/- 0.3 fmol/10(6) cells to 9.8 +/- 3.6 fmol/10(6) cells (p less than 0.1) and 24 h after a single injection the Bmax was maximally increased to 12.7 +/- 5.5 fmol/10(6) cells (p less than 0.05). The Kd was similar at all time points (about 3-5 nM). Furthermore, the specific insulin receptor binding was increased in adipocytes from estrogen treated rats. The specific insulin binding was maximally increased by 149 +/- 6% (p less than 0.001) after 4 days of daily estrogen injections. The increased binding seemed to be due to an increased number of insulin receptors on adipocytes from estrogen treated rats with no alteration of the ED50 value. In conclusion it was found that estrogen treatment has a positive feedback effect on its own nuclear receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1992

Biosynthetic capacity and regulatory aspects of prostaglandin E2 formation in adipocytes.

In contrast to previous studies, Parker et al. (Diabetes (1989) 38, 1123) have recently found that isolated rat adipocytes alone were unable to synthesize prostaglandins (PG) and that the PG measured in adipocyte suspensions were due to contaminating non-adipocyte cells. In the present study the capacity of adipocytes to produce PGE2 has further been explored. Preparations of isolated rat adipocytes were extensively washed in order to get rid of contaminating cells. The released PGE2 was measured by radioimmunoassay (RIA) after high-performance liquid chromatography (HPLC) separation. We found that after repetitive washing (up to 20 times) the isolated adipocytes were still able to synthesize PGE2 and this process was fully activatable by epinephrine, which indicates that pure adipocytes, themselves, are able to produce PGE2. However, addition of non-adipocyte material (from the adipose tissue) to 'pure' adipocytes (washed 10 times) enhanced the PGE2 synthesis significantly (P less than 0.001) as compared to 'pure' adipocytes alone. Thus, some kind of synergy exists between adipocytes and non-adipocyte cells in the adipose tissue in respect to PG formation. Some regulatory aspects of PG synthesis in 'pure' adipocytes were also investigated. Phospholipase A2 (2 U/ml) enhanced PGE2 synthesis significantly (119 +/- 21 to 658 +/- 85 pg/10(6) cells, P less than 0.001) without affecting lipolysis (glycerol release). The combined effect of epinephrine (5 microM) and phospholipase A2 (2 U/ml) on PGE2 formation was almost additive. Insulin inhibited the epinephrine-induced PG formation (P less than 0.01) but had no effects on the action induced by phospholipase A2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Deaminase↗
PubMed1992

Increased ornithine decarboxylase activity in kidneys undergoing hypertrophy in experimental diabetes.

Renal hypertrophy and hyperfiltration are early manifestations of human and experimental diabetes that may contribute to the late development of diabetic nephropathy. The biochemical events resulting in kidney growth in the diabetic state are completely unknown. Since growth of various tissues is accompanied by increased formation of polyamines, we studied whether polyamines were involved in the growth of the kidney observed in diabetic rats. This was done by measuring the activity of the rate-limiting enzyme in the polyamine pathway (ornithine decarboxylase; ODC) in kidneys from control, diabetic and insulin-treated diabetic animals. The ODC activity in the kidney was increased in the diabetic animals with a maximal rise 24 h after diabetes induction (6-fold, P less than 0.01); the activity thereafter declined. However, on day 14 the activity was still significantly elevated (2.5-fold, P less than 0.05). In insulin-treated diabetic animals the kidney ODC activity was only increased 3-fold (P less than 0.05) after 24 h, and for the rest of the study period the activity was about 1.8-fold higher than in control rats. After 14 days the kidneys from diabetic rats were significantly larger than kidneys from both control and insulin-treated diabetic rats, 1066 +/- 43 mg vs. 904 +/- 16 mg and 959 +/- 36 mg, respectively (P less than 0.01). For comparison, the ODC activity was also investigated in muscle. However, in muscle from diabetic animals the ODC activity declined steadily during the 14 days to 34% of control values (P less than 0.01), and insulin treatment completely normalized the ODC activity in muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Nuclear estradiol binding in rat adipocytes. Regional variations and regulatory influences of hormones.

The nuclear estrogen receptor was characterised in isolated rat adipocytes. The binding reaction with [3H]estradiol was performed with intact isolated rat adipocytes and the radioactivity associated with the nucleus was subsequently determined after cell lysis. The nuclear uptake of [3H]estrogen in rat adipocytes was temperature dependent and steroid specific. The steady-state binding was achieved after 30 min at 37 degrees C and was constant for several hours. Estradiol was found to bind to a homogeneous class of nuclear receptors in epididymal adipocytes with an apparent Kd of 3.1 +/- 0.76 nM and a Bmax of 7.98 +/- 1.11 fmol/10(6) cells corresponding to about 4800 receptors per nucleus. The estradiol binding exhibited regional variations in isolated adipocytes. In lean rats the highest receptor number was found in epididymal adipocytes, whereas there was a significantly lower number of nuclear binding sites in perirenal and subcutaneous adipocytes (P less than 0.05), unlike in older and more obese rats where the nuclear estradiol binding was greatest in adipocytes from the perirenal fat depot. Incubations with isoproterenol (10 microM) and dibutyryl-cAMP (2.5 mM) both reduced estradiol binding by 56% (P less than 0.005), while insulin (1 nM) enhanced the estradiol binding by 37% (P less than 0.01). In conclusion, a specific and high affinity nuclear estradiol receptor was demonstrated in rat adipocytes and regional differences in nuclear estradiol binding were detected. Furthermore, it was demonstrated that nuclear estradiol binding could be modulated by other agents known to affect adipocyte metabolism.

Adipose Tissue↗