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S Edén

Publications and source records attributed to S Edén.

At least 37 records · Page 2Linked to original sources

Additive effects of growth hormone and testosterone on lipolysis in adipocytes of hypophysectomized rats.

The effects of growth hormone (GH) and testosterone, alone or in combination, on the regulation of lipolysis in isolated adipocytes from hypophysectomized rats were investigated. Male Sprague-Dawley rats were hypophysectomized at 50 days of age. One week after operation, hormonal replacement therapy with L-thyroxine and hydrocortisone acetate was given to hypophysectomized rats. Groups of rats were treated with GH (1.33 mg/kg, daily), testosterone (10 mg/kg, once) alone or in combination. After one week of hormonal treatment, adipocytes were isolated from the pooled epididymal and perirenal fat pads and glycerol release after isoproterenol stimulation and 125I-cyanopindolol binding was measured. Hypophysectomy caused a marked decrease in basal and isoproterenol-stimulated lipolysis. There was no effect of testosterone treatment alone on lipolysis, but GH treatment resulted in an increase in isoproterenol-induced lipolysis but not to the levels observed in cells from control rats. Testosterone and GH in combination restored the lipolytic response to isoproterenol. Also 125I-cyanopindolol binding was decreased after hypophysectomy. Testosterone treatment alone and GH treatment alone increased the binding, while in combination the treatment had an additive effect. Affinity was not changed, but the effects seemed to be on receptor number, as determined by Scatchard analysis. Forskolin-stimulated cAMP accumulation in adipocytes was markedly reduced after hypophysectomy. Testosterone treatment alone had no effect. GH treatment alone increased forskolin-stimulated cAMP accumulation, although the level was lower than that found in control rats. The combined treatment resulted in a further increase to levels observed in adipocytes from control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipocytes↗

Prevalence of serum antithyroid peroxidase antibodies in 85-year-old women and men.

Antithyroid peroxidase antibodies (TPOAb) were determined by competitive radioassay in serum samples obtained from a representative population of 85-year-olds (601 women and 285 men). The prevalence of increased TPOAb concentration was significantly higher in the women. In individuals without previously known thyroid dysfunction, 16% of the women and 9% of the men had TPOAb concentration > 100 kilo-units/L, the upper decision limit. We found a direct relationship between TPOAb and thyrotropin (TSH) concentrations and an inverse relationship between TPOAb and free thyroxine (T4) concentrations, but no relationship between TPOAb and defined disorders or treatment with pharmaceutical drugs. Exclusion of individuals with increased TPOAb concentration and conditions influencing TSH and free T4 concentrations resulted in a decrease of the upper reference limit for TSH concentration and an increase of the lower limit for free T4 concentration, indicating that high TPOAb concentration should be taken into account when evaluating normal reference intervals for thyroid-function tests in the elderly.

Aged↗

Reduced hepatic growth hormone (GH) receptor gene expression and increased plasma GH binding protein in experimental uremia.

In uremia, reduced longitudinal growth and decreased hepatic insulin-like growth factor-I (IGF-I) secretion despite elevated GH serum levels point to an insensitivity to the action of GH. The molecular basis that accounts for this insensitivity could comprise decreased GH receptor expression in the target organs for GH or binding of GH in the circulation to substances that compete with the receptor. To address this hypothesis, the abundance of hepatic GH receptor mRNA was measured by solution hybridization RNase protection assay in uremic female Sprague-Dawley rats, following two-stage 5/6 nephrectomy, and in pair-fed and in ad libitum-fed sham-operated controls; rat GH binding protein (GHBP) plasma concentration was measured by a sensitive direct RIA. Uremia was associated with a 50% decrease of hepatic GH receptor expression compared to pair-fed controls, which themselves showed a 25% reduction of hepatic GH receptor mRNA abundance when compared to ad libitum-fed controls. Plasma GHBP levels in uremia were markedly higher than in both control groups. Treatment with recombinant human GH (rhGH) (10 IU/kg body wt per day s.c. for 10 days) led to a comparable induction of IGF-I plasma levels and weight gain in uremia and pair-fed controls, indicating that the insensitivity to GH in uremia can be overcome by large rhGH doses. Subcutaneous rhGH injections did not significantly alter the hepatic GH receptor transcript abundance or plasma GHBP levels in any of the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Low dose continuously infused growth hormone results in increased lipoprotein(a) and decreased low density lipoprotein cholesterol concentrations in middle-aged men.

OBJECTIVE: Animal studies have shown that slight increases in basal GH concentrations may result in changes in lipoprotein metabolism. Such changes in GH secretion have been observed in physiological and pathophysiological states such as fasting, uncontrolled diabetes and during oestrogen treatment. The aim of this study was to investigate the possible effects of increases in basal plasma GH concentrations on lipoprotein concentrations. DESIGNS: Recombinant human growth hormone (rhGH) was given as a continuous subcutaneous infusion in a low dose (0.02 U/kg/day) in an open study. PATIENTS: Eight middle-aged (42-59 years) overweight (body mass index: 26.1-33.8 kg/m2) but otherwise healthy men were studied over a period of 14 days. MEASUREMENTS: Blood samples were obtained after an over-night fast before and after 2, 7 and 14 days of treatment. Plasma and serum were separated and used for subsequent measurements of hormone and lipoprotein concentrations. On days 0, 7 and 14 of treatment, post-heparin plasma was also obtained for determinations of plasma lipoprotein lipase and hepatic lipase activities. In addition, a hyperinsulinaemic euglycaemic glucose clamp was performed on days 0 and 13 of the study. Fat biopsies from abdominal and gluteal fat depots were obtained for measurement of lipoprotein lipase activities on days 0 and 14 of the study. RESULTS: Serum GH concentrations increased to a steady level of 2-4 mU/l during treatment. Serum insulin-like growth factor-I (IGF-I) concentrations increased throughout the treatment period to twice the pretreatment levels. Plasma insulin and blood glucose concentrations increased on day 2 of treatment. After 7 and 14 days of treatment blood glucose concentrations were not different from pretreatment levels, but plasma insulin concentrations were still elevated. Serum cholesterol and low density lipoprotein (LDL) cholesterol concentrations had decreased after 7 and 14 days of treatment. High density lipoprotein (HDL) cholesterol concentrations were not affected, but very low density lipoprotein (VLDL) cholesterol and triglyceride concentrations increased transiently at day 2 of treatment. Serum apolipoprotein (apo) A-I, apoB and apoE concentrations were not significantly affected. Serum lipoprotein(a) concentrations had increased by days 7 and 14 to 147 and 142% of pretreatment concentrations, respectively. Lipoprotein lipase and hepatic lipase activities in post-heparin plasma, as well as abdominal and gluteal adipose tissue lipoprotein lipase activities, were not affected. There was no significant change in glucose disposal rate estimated from the glucose clamp studies. CONCLUSIONS: A low dose infusion of GH results in marked changes in lipoprotein concentrations with a transient increase in VLDL cholesterol and thereafter in a decrease in LDL cholesterol. In addition, this low dose of GH resulted in marked increases in lipoprotein(a) concentrations. The observed effects of GH may partly involve changes in IGF-I and insulin secretion.

Adult↗

Cardiovascular and renal effects of growth hormone.

OBJECTIVE: With the advent of recombinant human GH (rhGH), it has become possible in controlled clinical studies to explore the effects of GH replacement in adults with GH deficiency. The objective of this study was to determine cardiovascular and renal effects of GH replacement in adults with GH deficiency. PATIENTS: We studied ten patients (one woman and nine men), mean age 47 years, with GH deficiency. DESIGN: The patients were given s.c. rhGH (Humatrope, Eli Lilly) 0.5 U/kg/week or placebo in a 6-month double blind cross-over study. Cardiac and renal function was measured before drug administration (baseline), before cross-over (i.e. after 6 months), and before termination of drug administration (after another 6 months). Analysis of variance was used to compare measurements during GH replacement with baseline and placebo measurements. One patient was excluded because of atrial fibrillation. MEASUREMENTS: Main outcome measures were glomerular filtration rate and Doppler-echocardiographic estimates of cardiac function and structure. Computerized exercise electrocardiogram, spirometry, and blood samples for analyses of plasma hormones were also obtained. RESULTS: Left ventricular function was maintained during GH replacement. However, left ventricular mass increased from 211 to 249 g (P < 0.05) mainly due to increased left ventricular dimension since wall thicknesses did not increase. The left atrium increased from 38 to 41 mm (P < 0.05), possibly because stroke volume increased from 92 to 118 ml (P < 0.0001) and cardiac output increased from 5.29 to 7.58 l/min (P < 0.05). Total peripheral resistance decreased from 18.9 to 12.4 mmHg min/l (P < 0.05), and diastolic blood pressure from 79 to 72 mmHg (P < 0.05). Heart rate at rest increased from 58 to 70 beats/min. Systolic blood pressure at rest was unchanged, as was systolic blood pressure during dynamic exercise. GH replacement did not cause ST-abnormalities. Serum creatinine decreased from 91.4 to 85.3 mumol/l (P < 0.05) and glomerular filtration rate increased from 89.6 to 99.8 ml/min (P < 0.01). CONCLUSIONS: Thus, GH replacement has favourable cardiovascular and renal effects including increase of stroke volume and glomerular filtration rate with reduction of peripheral resistance.

Adult↗

Endotoxin levels in sera of elderly individuals.

The endotoxin levels in serum of 377 72-year-old individuals were quantitated. The study population was a representative sample of this age group and was participating in a general study of health and disease among the elderly in Göteborg, Sweden. The endotoxin levels in serum were quantified by the chromogenic Limulus amebocyte lysate assay and were correlated with the health status and laboratory findings for each individual. The mean endotoxin levels (+/- 1 standard deviation) in men and women, when excluding four outliers, were 6.6 +/- 3.8 and 6.9 +/- 3.8 pg/ml, respectively. All included, 21.5% of individuals had endotoxin levels equal to or above the sensitivity limit of 10 pg/ml. Strong positive correlations were found between endotoxin levels and plasma triglycerides (P > 0.995) and between endotoxin levels and serum protein (P > 0.9875). The endotoxin activity also correlated with mean corpuscular hemoglobin concentration (P < 0.005, negative correlation), body mass index (P > 0.9875), and decreased appetite (P > 0.9875). A high alcohol consumption was associated with increased endotoxin levels (P = 0.995). There are no previous studies which examine endotoxin levels in serum samples from individuals representative of the population. This study showed that elderly individuals had the same mean level of endotoxin as has been found in other age groups. The increased endotoxin levels seen in heavy drinkers may be explained by a decreased ability of the liver to remove endotoxin. The correlations found between endotoxin and triglycerides, protein, mean corpuscular hemoglobin concentration, decreased appetite, and body mass index are discussed.

Aged↗

Continuous but not intermittent administration of growth hormone to hypophysectomized rats increases apolipoprotein-E secretion from cultured hepatocytes.

Hypophysectomy of female rats has been shown to decrease the serum levels of apolipoprotein E (apoE). Continuous but not intermittent administration of GH to hypophysectomized (HX) rats increases these levels to those of normal rats, indicating that the sexually dimorphic secretion of GH is important in the regulation of apoE metabolism. In this study, these effects of GH were further investigated by studying the biosynthesis and secretion of apoE from isolated hepatocytes. Hepatocytes were isolated from HX rats as well as from HX rats that had received hormonal treatment with T4 and cortisol (C) or T4 and C together with GH given either as two daily sc injections (GH x 2) or as a continuous infusion (GHc). Hypophysectomy decreased by 47% the amount of apoE present in the culture medium after a 4-h incubation. Treatment of HX rats with T4 and C alone or in combination with GH x 2 did not influence the amount apoE present in the medium, whereas treatment with T4, C, and GHc increased the amount of apoE to that of normal controls. The different levels of apoE in the medium was not due to differences in the disappearance of apoE, indicating that it was caused by changes in the rate of apoE secretion. Consistent with this, hypophysectomy decreased the rate of intracellular accumulation of apoE measured by incubation of the cells with [35S]methionine for 0, 8, and 20 min. Treatment with T4, C, and GHc increased the rate of accumulation, but T4, C, and GH x 2 had no effect. The differences in the initial rate of intracellular accumulation of apoE were not due to variations in apoE messenger RNA pools or to differences in the degradation of apoE at a step early in the secretory pathway. These results indicate that the differences in the initial rate of accumulation of apoE results from differences in the translational rate. The major amount of apoE that was secreted to the medium appeared in the high-density lipoprotein fraction, whereas small amounts were present in the very-low-density lipoprotein fraction (VLDL). Hypophysectomy decreased the amount of newly secreted apoE in the VLDL fraction. Only therapy with T4, C, and GHc could restore the normal distribution of apoE in the VLDL fraction. In conclusion, the results indicate that the secretory pattern of GH is involved in the regulation of the apoE secretion by influencing the rate of translation.

Animals↗

Insulin-like growth factor-I and growth hormone have different effects on serum lipoproteins and secretion of lipoproteins from cultured rat hepatocytes.

GH has previously been shown to regulate serum lipoprotein levels and hepatic secretion of apolipoprotein-B (apo-B) and apo-E in the rat. The aim of this investigation was to study a possible role of insulin-like growth factor-I (IGF-I) in this regulation. Adult female rats were hypophysectomized and treated with recombinant human IGF-I (1.25 mg/kg.day) as a sc continuous infusion for 7 days. The effects of IGF-I were compared with those of bovine GH, given either as a continuous sc infusion or as two daily sc injections. All hypophysectomized rats were given replacement therapy with L-T4 and cortisol. Serum IGF-I concentrations increased to similar levels as a result of treatment with bovine GH and IGF-I. There was no effect of IGF-I on serum concentrations of glucose or insulin, whereas GH, independent of its mode of administration, increased serum insulin concentrations. Food intake was not affected by treatment with IGF-I. IGF-I had no effect on serum concentrations of cholesterol or apo-E, whereas GH given twice daily decreased serum cholesterol concentrations, and a continuous infusion of GH increased serum apo-E concentrations. Serum triglyceride and apo-B concentrations increased markedly as a result of IGF-I treatment, whereas GH had no effect on serum triglycerides, but decreased serum apo-B concentrations. Hepatocytes were isolated from hypophysectomized rats treated with L-T4 and cortisol alone or in combination with IGF-I and kept in short term cultures. In this system, IGF-I had no effect on the incorporation of [3H]glycerol in triglycerides or the mass of triglycerides in the cells and medium. There was no effect of IGF-I treatment on the secretion of apo-E or apo-B. Moreover, there was no effect of IGF-I treatment on the relationship between newly synthesized and secreted apo-B 48 and apo-B 100, as determined by [35S]methionine labeling of the proteins. In conclusion, the previously observed effects of GH on serum lipoproteins and hepatic apolipoprotein secretion does not seem to be mediated via IGF-I, but IGF-I has its own unique effects on serum triglyceride and apo-B levels. The increases in serum apo-B and serum triglyceride concentrations after IGF-I treatment were not dependent on increased hepatic secretion of apo-B or triglycerides.

Animals↗

Estradiol regulation of mRNA expression of stimulatory G-protein alpha-subunit in white adipose tissue from female rats.

Adipose tissue has been recognized as a major peripheral metabolic target of estrogens. The present study was addressed to examine in female rats whether differences in the adipose tissue mRNA expression of alpha-subunit of stimulatory (Gs) and/or inhibitory (Gi) G-proteins exist between intact and ovariectomized rats, the latter with or without estradiol or testosterone treatment. The fat cell membrane protein amount of Gs and Gi alpha-subunit also was examined. All these parameters were evaluated in parametrial fat tissue samples obtained from 40 female Sprague-Dawley rats. A group of rats (N = 20) was investigated for evaluation of mRNA expression and another group (N = 20) for quantification of the protein amount of Gs and Gi alpha-subunit. Each group was represented by five control rats (sham-operated), five ovariectomized (OVX) rats, five ovariectomized rats treated with estradiol (OVXE) and five ovariectomized rats treated with testosterone (OVXT). Ribonucleic acid extracted from adipose tissue and analyzed by northern blot with G alpha s, G alpha i-3 cRNA probes revealed three major bands with estimated sizes of 1.9, 3.5 and 2.35 kb, respectively. Messenger RNA quantitative analysis, by a solution of hybridization RNAase protection assay on total nucleic acid samples, showed that the amount of G alpha i-1 and G alpha i-2 mRNA was similar within the different groups, whereas the G alpha s mRNA was significantly less abundant (p < 0.01) in OVX and OVXT rats than in control or OVXE rats. No difference in G alpha s mRNA content was found between control and OVXE rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Growth hormone but not gonadal steroids influence lipoprotein lipase and hepatic lipase activity in hypophysectomized rats.

Lipoprotein lipase and hepatic lipase are involved in the degradation and cellular uptake of lipids in peripheral tissues and the liver. These enzymes seem to be influenced by gonadal steroids in the rat as well as in man. Since gonadal steroids have been shown to influence the secretory pattern of GH and since the effect of gonadal steroids on several metabolic functions may be dependent upon their effects on GH secretion, the present study was undertaken to investigate the developmental regulation of heparin-releasable lipoprotein lipase and hepatic lipase activities in female and male rats, and to study the effects of gonadal steroids and different modes of GH administration to hypophysectomized rats on these enzyme activities. Female and male Sprague-Dawley rats from 20 to 65 days of age were studied. Hypophysectomy was performed at 50 days of age and these rats were given replacement therapy with thyroxine and cortisone. Groups of hypophysectomized rats were treated with either oestradiol valerate (0.1 mg/kg per day) or testosterone enanthate (1 mg/kg per day). Bovine GH (1 mg/kg per day) was given to groups of hypophysectomized rats either by two daily subcutaneous injections or by continuous infusion using osmotic minipumps. Hormone treatment was given for 1 week. Lipoprotein lipase and hepatic lipase activities were measured in heparinized plasma. There was no difference in lipoprotein lipase activity between male and female rats at 20 to 45 days of age. Lipoprotein lipase activity decreased between 45 and 65 days of age in male rats but not in females and, at 65 days of age, lipoprotein lipase activity was higher in females compared with males.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations.

The effects of growth hormone treatment of adults with adult-onset pituitary insufficiency on lipoproteins and apolipoproteins were investigated. Nine patients, one women and eight men (age range, 34-58 years), who had been treated for pituitary tumors were studied. They had complete pituitary insufficiency with a duration of at least 1 year. All patients received replacement therapy with thyroid hormones, glucocorticoids, and gonadal steroids. The study had a double-blind, placebo-controlled, crossover design for active treatment with recombinant human growth hormone (0.25-0.5 units/kg per week s.c. given each evening) for 6 months. Fasting serum levels of cholesterol; triglycerides; high density lipoprotein and low density lipoprotein cholesterol; apolipoproteins A-I, B, and E; and lipoprotein (a) were measured before and after 6 and 26 weeks of treatment. Lipoprotein (a) concentrations increased markedly during treatment and were about twice as high compared with pretreatment levels. Serum cholesterol and low density lipoprotein cholesterol concentrations were decreased after 6 weeks of treatment, but levels had returned to pretreatment levels after 26 weeks. High density lipoprotein cholesterol concentrations increased during treatment and were significantly higher than pretreatment levels after 26 weeks of treatment. Serum triglyceride concentrations did not change significantly, but in two patients with marked hypertriglyceridemia, growth hormone treatment resulted in a marked decrease. Serum concentrations of apolipoproteins A-I, B, and E did not change significantly, but changes in apolipoprotein A-I and B concentrations were in parallel to those observed for high density lipoprotein cholesterol and low density lipoprotein cholesterol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Postreceptor events involved in the up-regulation of beta-adrenergic receptor mediated lipolysis by testosterone in rat white adipocytes.

In the previous studies we have shown that testosterone increases lipolytic responsiveness to catecholamines in rat white adipocytes, and that is associated with an up-regulation of beta-adrenergic receptor density. However, the postreceptor events involved in the testosterone induced enhancement of beta-adrenergic receptor activated lipolysis in these cells have not been adequately studied, and were therefore investigated in the present study. Male Sprague Dawley rats were divided into three groups: control, castrated, and castrated treated with testosterone. The beta-adrenergic receptor-mediated cAMP accumulation, measured with RIA after isoproterenol (a beta-adrenergic agonist) stimulation was decreased in castrated rats, and reversed by testosterone treatment, suggesting a testosterone effect at or proximal to adenylate cyclase. However, no differences between the groups were found in abundance of G alpha protein messenger RNAs (G alpha s, G alpha i-1, and G alpha i-2) as analyzed by Northern blot and a solution hybridization RNase protection assay, or in G protein mass measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation. Lipolysis stimulated by N6-monobutyryl-cAMP was reduced in castrated rats and recovered by testosterone treatment, suggesting that components distal to the adenylate cyclase, i.e. protein kinase A (PKA) and/or hormone sensitive lipase (HSL) also are involved in testosterone regulation of lipolysis. In conclusion, these and previous results suggest that the testosterone-induced increase in lipolytic response to catecholamines in rat white adipocytes is mediated through several events including an increased beta-adrenergic receptor density, probably an increased adenylate cyclase activity and an increased protein kinase A/hormone sensitive lipase activity at the postreceptor level with apparent absence of effect on the expression of G-proteins.

Adenylyl Cyclases↗

Treatment of adults with growth hormone (GH) deficiency with recombinant human GH.

In a double blind, cross-over placebo-controlled trial, we studied the effects of 26 weeks of replacement therapy with recombinant human GH on body composition, metabolic parameters, and well-being in 10 patients with adult-onset GH deficiency (GHD). All patients received appropriate thyroid, adrenal, and gonadal replacement therapy. The dose of recombinant human GH was 0.25-0.5 U/kg.week (0.013-0.026 mg/kg.day) and was administered sc daily at bedtime. One patient was withdrawn from the study because of edema and atrial fibrillation. Body composition was estimated with three independent methods: computed tomography, bioelectric impedance, and total body potassium combined with total body water assessments. The Comprehensive Psychological Rating Scale and the Symptom Check List-90 were used to assess any change in psychopathology. After 26 weeks of treatment, adipose tissue (AT) mass decreased 4.7 kg (P < 0.001). Subcutaneous AT decreased by an average of 13%, whereas visceral AT was reduced by 30%. Muscle volume increased by 2.5 kg (5%; P < 0.05). According to the four-compartment model derived from assessments of total body potassium and total body water, body cell mass and extracellular fluid volume increased significantly by 1.6 and 3.0 kg, whereas body fat decreased by 6.1 kg. Results obtained by the bioelectric impedance technique were similar. The mean (+/- SD) concentrations of insulin-like growth factor-I increased from 0.26 (0.06) at baseline to 2.56 (1.55) and 2.09 (1.03) kU/L after 6 and 26 weeks of treatment. Calcium and serum phosphate, osteocalcin, and procollagen-III concentrations were significantly higher, and intact PTH concentrations were reduced after 6 and 26 weeks of treatment, respectively. Total and free T3 concentrations were significantly increased after 6 and 26 weeks of treatment, whereas free T4 concentrations were reduced at 6 weeks, but after 26 weeks, free T4 concentrations had returned to pretreatment values. Finally, after 26 weeks of treatment, there was a decrease in the Comprehensive Psychological Rating Scale score (P < 0.05). The results show that GH replacement in GHD adults results in marked alterations in body composition, fat distribution, and bone and mineral metabolism and reduces psychiatric symptoms. Finally, we conclude that the observed beneficial effects of replacement therapy with GH are of sufficient magnitude to consider treatment of GHD adults.

Adipose Tissue↗

Cardiovascular risk factors in adult patients with growth hormone deficiency.

Patients with adult onset growth hormone deficiency have a decreased life expectancy owing to an increased mortality from cardiovascular disease. In the present study, 104 subjects (66 men and 38 women, aged 22-74 years) with growth hormone deficiency and with adequate replacement therapy with glucocorticoids, thyroid hormones and gonadal steroids were studied with respect to known risk factors for cardiovascular disease. For comparison, data from a population study, "the MONICA study", were obtained. The patients had a significantly higher body mass index compared to controls (p < 0.001). Serum triglyceride concentration was higher (p < 0.001) but there was no difference in serum total cholesterol concentration. Serum high-density lipoprotein cholesterol concentration was lower (p < 0.001) in the patients. There was no difference in the prevalence of diabetes mellitus. The prevalence of treated hypertension was higher (p < 0.05) in the patients but the prevalence of smoking was lower (p < 0.001). Even after taking the increased body mass index into consideration, the changes in the prevalence of treated hypertension (p < 0.05) and in the serum concentrations of triglycerides (p < 0.05) and high-density lipoprotein concentrations (p < 0.001) remained. These results indicate that growth hormone deficiency alters lipoprotein metabolism and increases the risk for development of hypertension, which in turn might contribute to the increased risk for cardiovascular disease.

Adolescent↗

The prevalence of radiographic osteoarthritis is low in elderly patients with growth hormone deficiency.

The prevalence of radiographic osteoarthritis in hand and knee joints was studied in elderly patients with acromegaly and growth hormone deficiency, respectively, and compared with a normal population of elderly people. There were no major differences in the prevalence of osteoarthritis between the acromegalics and the normal population, but the patients with growth hormone deficiency had significantly (p < 0.001) less osteoarthritis than the normal population. The lack of differences between the acromegalics and the normal population could be an effect of the age interval studied in which the prevalence of osteoarthritis is high. The low prevalence of osteoarthritis in patients with growth hormone deficiency suggests that growth hormone is an important factor in the development of osteoarthritis.

Acromegaly↗

Amount of G-protein alpha-subunit in rat white adipocytes: lack of difference between subcutaneous and visceral fat.

It has been the purpose of this study to examine possible differences in the amount of stimulatory (Gs) and inhibitory (Gi) G-protein alpha-subunits (measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation) between subcutaneous and intra-abdominal regions in rats. The lipolytic response to isoproterenol and the number of beta-adrenergic binding sites were also examined. These parameters were all evaluated simultaneously in subcutaneous (inguinal), epididymal and perirenal fat samples collected from six male Sprague-Dawley rats. The membrane contents of the Gs and Gi alpha-subunits were similar in the three depots. Moreover, no difference was found among the different regions with regard to isoproterenol-stimulated glycerol release and beta-adrenoceptor number, expressed per cell number. In conclusion, the present study shows for the first time in rats that the abundance of inhibitory and stimulatory G-protein alpha-subunits is similar in subcutaneous and in visceral adipocytes. Moreover, the number of beta-adrenoceptors and the lipolytic response to isoproterenol do not show significant variations with the anatomical site. As the present results are apparently in contrast with those obtained previously in human adipocytes, there is a possibility that the different results observed in rat and in human fat cells could be explained by species differences.

Adipose Tissue↗