Preliminary studies on the reaction of growing geese (Anser anser f. domestica) to the proximity of wind turbines.

Wind farms produce electricity without causing air pollution and environmental degradation. Unfortunately, wind turbines are a source of infrasound, which may cause a number of physiological effects, such as an increase in cortisol and catecholamine secretion. The impact of infrasound noise, emitted by wind turbines, on the health of geese and other farm animals has not previously been evaluated. Therefore, the aim of this study was to determine the effect of noise, generated by wind turbines, on the stress parameters (cortisol) and the weight gain of geese kept in surrounding areas. The study consisted of 40 individuals of 5-week-old domestic geese Anser anser f domestica, divided into 2 equal groups. The first experimental gaggle (I) remained within 50 m from turbine and the second one (II) within 500 m. During the 12 weeks of the study, noise measurements were also taken. Weight gain and the concentration of cortisol in blood were assessed and significant differences in both cases were found. Geese from gaggle I gained less weight and had a higher concentration of cortisol in blood, compared to individuals from gaggle II. Lower activity and some disturbing changes in behavior of animals from group I were noted. Results of the study suggest a negative effect of the immediate vicinity of a wind turbine on the stress parameters of geese and their productivity.

25(OH)D3 in patients with ovarian cancer and its correlation with survival.

OBJECTIVES: The aim of this study was to examine vitamin 25(OH)D3 concentration in ovarian cancer patients in relation to a pathological subtype of the tumor, FIGO stage, grading, menopause status and overall 5-year survival. DESIGN AND METHODS: 72 epithelial ovarian cancer patients aged 37-79, who undergone optimal cytoreductive surgery were enrolled to the study group. Serum 25(OH)D3 concentration was measured using an electrochemiluminescence immunoassay before surgery. Serum concentration of 25(OH)D3 was also measured in a group of 65 healthy non-obese women aged 35-65 years. RESULTS: In patients with ovarian cancer serum concentration of 25(OH)D3 was lower than in the reference group (12.5±7.75 ng/mL vs 22.4±6.5 ng/mL). No significant correlation was found between serum 25(OH)D3 concentration and histological subtype, grading, FIGO stage and menopausal status. The study group was divided into two subgroups and the survival curves were analyzed. Overall 5-year survival rate was significantly higher in the subgroup of patients with 25(OH)D3 concentration over 10 ng/mL compared to women with concentration below 10 ng/mL. CONCLUSIONS: Low 25(OH) D3 concentration associated with lower overall survival rate might suggest for the important role of severe deficiency in more aggressive course of ovarian cancer. Testing for 25(OH)D in the standard procedure could help to find ovarian cancer patients with worse prognosis, who would benefit of special attention and supplementation.

Long-term weight gain and metabolic syndrome, adiponectin and C-reactive protein in women aged 50-60 years.

PURPOSE: The aim of this study was to determine the impact of the weight change during 30-40 year follow-up on the prevalence of metabolic syndrome (MS) components, C-reactive protein (CRP) and adiponectin. MATERIAL AND METHODS: The study included 153 women. Blood pressure, anthropometric and laboratory measures were done at the age of 50-60 years. All women declared normal body weight at age 20. The MS was defined according to the International Diabetes Federation (IDF 2005). Women were divided into four groups according to weight gain: < 10 kg, 10-19 kg, 20-29 kg, > 30 kg. RESULTS: The highest values of waist circumference, BMI, WHR, CRP, glucose, HOMA index, insulin, triglycerides, blood pressure and the lowest concentrations of adiponectin and HDL-cholesterol were observed in the group with the highest weight gain (above 30 kg). Odds ratio for MS was tenfold higher in group with weight gain 10-19 kg and 20-29 kg and twenty fold higher in group with weight gain above 30 kg. In multiple regression analysis CRP was most significantly correlated with weight gain. CONCLUSIONS: Among biochemical parameters of metabolic syndrome CRP seems to be the most significantly related to weight gain. The risk of metabolic syndrome is significantly increased even when the weight gain is 10 kg in middle-aged women characterized by a normal BMI at the age of 20.

Serum Adiponectin and Indices of Cardiovascular Risk in Young Women with Excessive Body Mass.

Adiponectin reduces oxidative stress, the release of C-reactive protein and influences on the process of atherogenesis reducing lipid accumulation in the blood vessels. The findings on the association of adiponectin with cardiovascular risk are contradictory. This study aimed to assess the relationship between adiponectin and indices of cardiovascular risk in women with excessive body mass. Adiponectin, hsCRP and lipids were measured in blood samples obtained from normoglycemic women with excessive body mass (n=52;BMI≥25 kg/m(2)) aged 25-40 yrs and age-matched healthy controls (n=36; BMI<25kg/m(2)). All subjects underwent blood pressure examination and anthropometric measurements. Median concentration of adiponectin in the serum in women with excessive body mass was significantly lower than in women with normal weight (10,8 vs 15,5 µg/ml; p<0,01). Similarly, median serum concentration of triglycerides, hsCRP and blood pressure values were significantly higher and HDL-cholesterol significantly lower in women with BMI≥25 kg/m(2) in comparison to these with normal BMI, however only HDL-C and hsCRP were found to be beyond widely accepted cut-offs. Hypoadiponectinemia in women with excessive body mass (adiponectin concentration below the 5(th) percentile in the control group) was associated predominantly with abnormally increased median values of hsCRP and blood pressure. Concentrations of total cholesterol, non-HDL-C and LDL-C were also significantly higher in women with excessive body mass and hypoadiponectinemia, however still within the reference range. Our results suggest that adiponectin may be used as a prognostic marker of cardiovascular risk in women with excessive body mass.

Menstrual cycle in women addicted to alcohol during the first week following drinking cessation--changes of sex hormones levels in relation to selected clinical features.

AIMS: To assess the prevalence of hormonal dysfunction in women addicted to alcohol during first week following drinking cessation; to determine whether fluctuations of hormone levels in follicular, ovulation and luteal phases in addicted women are equal to those normally found in healthy women; to determine the association between hormonal imbalances with selected clinical features. METHODS: Biochemical parameters of liver function and hormone levels were assessed in 30 women treated for 30 days in a Short Term Therapy and Detoxification Ward. The following hormones were measured: prolactin (PROL), folliculotropin (FSH), luteotropin (LH), estradiol (ES) and testosterone (TEST)--(i) after menstruation, at follicular phase, between 5th and 7th day of the cycle; (ii) around ovulation, 11-14th day of the cycle; and (iii) before menstruation, at luteal phase, between 19th and 22th day of the cycle. RESULTS: Mean PROL levels in all three cycle phases and progesterone level in follicular phase were above, while mean TEST level was below, the reference values. Over 50% of women had abnormally increased PROL values in all phases of the cycle while decreased values of PROG or LH were found in approximately 50% and >30% of study women. CONCLUSIONS: The menstrual cycle disturbances in alcoholic women are most prominent around the middle part of the cycle and age influences the pattern of hormonal changes.

Markers of pro-inflammatory and pro-thrombotic state in the diagnosis of metabolic syndrome.

The metabolic syndrome refers to the clustering of upper body obesity, atherogenic dyslipidemia, insulin resistance and elevated blood pressure. Both, obesity and metabolic syndrome, have the potential to influence on the incidence and severity of cardiovascular disease with serious implications for worldwide health care systems. Obesity plays a central role in the development of insulin resistance and dyslipidemia through the mediation of a pro-inflammatory and pro-thrombotic state. Adipose tissue has been shown to exert important endocrine and immune functions. Pathogenesis of obesity associated metabolic syndrome is mediated by disturbed production and release of biologically active molecules by fat cells and other cells infiltrating fat tissue. In obese subjects synthesis of several bioactive compounds--adipokines and cytokines/chemokines by adipose tissue cells is dysregulated. Those bioactive molecules participate in regulation of apetite and energy homeostasis, lipid metabolism (tumour necrosis factor alpha--TNF-alpha), insulin sensitivity (TNF-alpha, adiponectin, resistin, visfatin) immunity (monocyte chemoattractant protein-1--MCP-1, TNF-alpha, IL-6), angiogenesis, blood pressure and hemostasis (plasminogen activator inhibitor--PAI-1). The effects of major pro-/anti-inflammatory and pro-thrombotic adipokines on several physiological processes will be discussed in this review. Also, an evidence-based approach to the laboratory diagnosis and treatment of metabolic syndrome will be presented.

Effect of sulodexide on albuminuria, NAG excretion and glomerular filtration response to dopamine in diabetic patients.

BACKGROUND: Albuminuria is the best and most readily available marker for glomerular damage and progressive renal function loss in patients with diabetic nephropathy. Recently, administration of the oral glycosaminoglycan sulodexide (a mixture of 80% fast-moving heparin and 20% dermatan sulphate) was shown to effectively decrease albumin excretion rate in diabetics with nephropathy. AIMS: To evaluate whether the hypoalbuminuric effect of sulodexide is associated with improvement of the renal vascular or tubule function. METHODS: Forty-five type 1 diabetic patients, affected by diabetic nephropathy with albuminuria for at least 5 years, were randomly allocated to sulodexide or untreated. Those allocated to sulodexide were given 100 mg of sulodexide daily for 120 days. Renal vascular function (DIR) and N-acetyl-beta-D-glucosaminidase (NAG) excretion were estimated before and at the end of the study, the former in thesulodexide group only. DIR was measured as two Cr(cl) lasting 120 min (before and during 2 mug/kg b.w. i.v. dopamine). RESULTS: The analysis of trends during the study demonstrated a marked reduction of albuminuria in the sulodexide group (from 126.1 +/- 15.41 to 93.6 +/- 13.7 mg/day). DIR rose from 13.2 +/- 2.1% to 15.44 +/- 1.9% (relative increase: +16.9%), and NAG excretion showed a decreasing trend decreased in the sulodexide group only (from 5.1 +/- 0.62 to 4.7 +/- 0.40 U/g(creat)). CONCLUSION: The findings presented in this study indicate for the first time that orally available sulodexide may favorably affect the renal vascular function in type 1 diabetic patients with nephropathy and microalbuminuria. The effect of sulodexide on NAG is strongly influenced by the baseline NAG values, with a significant NAG reduction in the patients with the highest baseline NAG values.

Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent restenosis -- comparison with stable and unstable angina.

OBJECTIVE AND DESIGN: It is believed that the magnitude of the systemic inflammatory response induced by percutaneous coronary intervention (PCI) impacts on the long-term outcomes in patients with stable angina (SA) and unstable angina (UA). We aimed to determine whether an inflammatory response appears in in-stent restenosis (ISR) patients undergoing balloon angioplasty and to assess its pattern and magnitude in relation to SA and UA subjects. SUBJECTS: 80 patients (59 with SA, 10 with UA, 11 with ISR) were enrolled into the prospective study. TREATMENT: SA and UA patients undergoing single vessel coronary balloon angioplasty followed by stenting versus ISR subjects in whom only balloon angioplasty was performed. METHODS: C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) were measured in blood samples collected before and 6, 24 h and 1 month after the procedure. RESULTS: A comparable pattern of inflammatory response in terms of CRP and SAA concentrations in subjects undergoing PCI due to ISR and SA was discovered while in unstable patients its magnitude was substantially higher. CRP and SAA levels increased significantly in each group with the peak value at 24 h and the baseline levels remarkably correlated with the highest markers' concentrations. In contrast, preprocedural TNF-alpha concentrations were higher in ISR group when compared with SA and UA patients. Additionally, in ISR group a twofold increase in their values of borderline significance at 6 h was noted. SA and UA subjects were found to have significantly lower TNF-alpha levels at 6 and 24 h after the intervention though the marker concentrations markedly increased with peak values at 1 month. The levels of IL-10 did not differ at any time point between the groups. CONCLUSIONS: We suggest that PCI triggers a systemic inflammatory response in patients with ISR and considerable differences in its pattern when compared with SA and UA patients were demonstrated. Moreover, a high preprocedural TNF-alpha level and its increase provoked by PCI in the ISR group warrant the need for further investigation of its possible involvement in the restenosis process.

Function, structure, and volume of thyroid gland following allogenic kidney transplantation.

The aim of the study was to assess the structure, volume, and function of the thyroid gland following kidney transplantation compared with those features of long-term transplant recipients as well as patients with normal native kidney function. Study group A consisted of 30 patients undergoing allogenic kidney transplantation, study group B included 30 long-term kidney transplant recipients who displayed stable renal function at 4 to 11 years following transplantation; control group C comprised 38 patients who were diagnosed or treated for reasons other than thyroid or renal insufficiency. Mean FT-3 concentrations in group A decreased from 2.19 pg/mL preoperatively to 1.52 pg/mL on the first posttransplantation day, returning to the preoperative values (2.06 pg/mL) at 30 days postoperatively. After 6 months the concentrations of thyroid hormones were similar to those among the long-term posttransplantation group (group B), although still lower than those in the control group. Mean thyroid volume in dialyzed patients was 17.10 mL; in the long-term group, 17.60 mL; and in the control group, 15.82 mL between groups that were not statistically significant. Abnormal structure of the thyroid gland was observed in 63% of group A (n = 19), 70% of group B (n = 21), and 29% of the control group. Significantly more abnormal thyroid gland structures were observed among dialyzed or transplanted patients. The thyroid volume was similar in all groups. Significant transient decrease in thyroid stimulating hormone (TSH) and free triidothyronine (FT-3) was not free thyroxine (FT-4) concentrations following kidney transplantation. Occasionally, increase accompanied by a change in FT-4 and TSH concentrations were observed, and antithyroid antibodies were detected only sporadically.

Parathormon, calcium, phosphorus, and left ventricular structure and function in normotensive hemodialysis patients.

Clinical and experimental data suggest that Parathormon (PTH), calcium, and phosphorus participate in left ventricular hypertrophy (LVH) and affect myocardial contractility in end-stage renal disease. Cellular calcium overload and interstitial fibrosis induced by PTH may lead to impairment of left ventricular diastolic function. Hyperphosphatemia is an independent risk of cardiovascular mortality in dialysis patients. The aim of the study was to estimate the influence of PTH and calcium-phosphorus metabolism on left ventricular structure and function in hemodialysis patients, without hypertension and antihypertensive drug therapy (SBP = 126.2 +/- 11.1 DBP = 75.8 +/- 6.5 mmHg). Echocardiographic findings in a group of 22 normotensive HD patients had been compared to 43 hypertensive HD patients. Relationships between PTH, calcium-phosphorus metabolism and echocardiography in normotensive group were then evaluated. Left ventricular mass index (LVMI) was lower in normotensive patients: 128.3 +/- 46.2 versus 165.8 +/- 46.7 (p < 0.01). The prevalence of LVH was 55% in normotensive HD patients compared to 86% in hypertensive group (p < 0.01). In normotensive group we found correlation between PTH and LVMI (r = 0.44; p < 0.05). There were also significant relationships between calcium and posterior wall thickness (r = -0.44; p < 0.05), phosphorus and LVMI (r = 0.47; p < 0.05). A significant correlation was observed between both phosphorus, calcium x phosphorus product and E/A ratio: r = -0.47 and r = -0.43, respectively (p < 0.05 both). Disturbances of calcium-phosphorus metabolism and secondary hyperparathyroidism contributes to left ventricular hypertrophy, and impaired left ventricular diastolic function in normotensive hemodialysis patients.

[Antibodies to tissue transglutaminase as marker of gluten-free diet maintenance in patients with coeliac disease]. / Przeciwciala przeciwko transglutaminazie tkankowej jako marker przestrzegania diety bezglutenowej u chorych na celiakie.

The aim of the study was to assess the compatibility of IgA antiendomysium antibodies (IgAEmA) and IgA tissue transglutaminase antibodies (IgAtTG) in treated patients with coeliac disease and to estimate the value of the IgAtTG-ELISA as a marker of gluten-free diet maintenance. The study included 71 children and young adults (46 F, 25 M) aged from 6 years to 27 years, on the gluten-free diet (in some cases unrestricted) for at least 4 years because of coeliac disease diagnosed according to ESPGHAN criteria. Serum samples of all patients were examined simultaneously for IgAEmA titer by indirect immunofluorescence and IgAtTG level by ELISA test. IgAEmA antibodies were present in 26 patients (36.6%). IgAtTG-ELISA were positive in 23 patients (32.4%), equivocal--in 8 patients (11.3%) and negative--in 40 patients (53.6%). The serological tests were compatible in 58 patients (81.7%). If we consider equivocal results of IgAtTG test to be negative, IgAEmA and IgAtTG tests will be compatible in 64 cases (90.1%). Tissue transglutaminase antibodies ELISA provide a sensitive test of the gluten-free diet maintenance in patients with coeliac disease.

Bone turnover markers and estradiol level in postmenopausal women.

It has been found recently that women with estradiol (E) levels < 5 pg/ml were more likely to suffer osteoporotic fractures. We evaluated the relationships between biomarkers of bone turnover and changes in hormone levels in early or late postmenopausal women without any replacement therapy. Follicle stimulating hormone (FSH), luteinizing hormones (LH), estradiol and serum resorption (crosslaps) and formation (osteocalcin) markers were assayed. Bone densities in the spine and femoral neck were also measured. Elevated FSH, LH and decreased estradiol in postmenopausal women were accompanied by higher osteocalcin (9.1-9.7 ng/ml) and crosslaps level (3305-3458 pmol/l) compared to premenopausal women (6.8 ng/ml and 2087 pmol/l). Bone density was lower in elderly women. A significant inverse correlation was found between estradiol and crosslaps level; FSH and LH were also correlated with bone markers. Estradiol levels < 9 pg/ml were associated with increased bone resorption, decreased hip bone density and higher frequency of osteopenia and osteoporosis. Over 57% of women with an estradiol < 9 pg/ml could be identified as having "a high turnover" compared with 30% with estradiol above 9 pg/ml. Our results indicate that changes in bone density may not be very clear but an increase in bone turnover is distinctly apparent in women with severe estradiol deficiency.

[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. / Czy istnieja zaleznosci pomiedzy niektórymi zaburzeniami metabolicznymi a wybranymi wskaznikami uszkodzenia nerek u chorych z nieleczonym pierwotnym nadcisnieniem tetniczym?

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).

Uptake of thyroxine by cultured human adipocyte precursors isolated from lean and obese subjects.

The mechanism of thyroxine uptake by human adipocyte precursors has been studied in primary culture. Also the rates of transport of this hormone into the isolated cells of adipose tissue were compared for lean and obese subjects. It was demonstrated that thyroxine transport into the human adipocyte precursor cells is an active, energy-dependent process characterized by very low rate (Km = 10 pmol/l, Vmax = 8 fmol FT4/10(6) cells/min.). By comparing the rates of thyroxine transport into the precursor cells of adipocytes isolated from adipose tissue of lean and obese subjects it was possible to demonstrate a clear tendency to the lowered rate of transport of thyroxine to the cells in obesity. The results of this study suggest that the lowered rate of thyroxine transport to preadipocytes and adipocytes observed in obesity may significantly influence the metabolic state of these cells.

[Regulation of triiodothyronine levels in fatty tissue in obese patients]. / Regulacja poziomu trijodotyroniny w tkance tluszczowej u ludzi otylych.

Specific activity of T4-5'-deiodinase, the enzyme which catalyze peripheral production of triiodothyronine (T3) from thyroxine (T4) has been evaluated in the subcutaneous adipose tissue of obese patients. In lean healthy women (BMI less than 21) mean activity of T4-5'-D was found to be 122 +/- 29.4 fmol T3/mg of protein/min and was higher then respective activity of the enzyme in adipocytes of patients with mild obesity (22 less than BMI less than 30) where the mean was 92.14 +/- 18.05 fmol T3/mg/min. The activity of T4-5'-D was significantly decreased in patients with severe obesity (BMI less than 30) when compared with respective activity of the enzyme found in controls (47.36 +/- 18.4 fmol T3/mg/min vs 122.4 +/- 29.4 fmol T3/mg/min; p less than 0.01). As T4-5'-D in human adipose tissue has been previously characterized as type II of the enzyme, diminished activity found in obese subjects means that thyroid metabolic activity of adipocyte is decreased. Such a state would lead to antilipolytic action of catecholamines in obesity.

Adipogenic activity in the plasma of genetically obese Zucker rats.

The potential of plasma to stimulate differentiation and lipid filling of adipose precursors in primary culture was investigated in the groups of genetically obese Zucker rats (fafa) and their lean littermates (FaFa). The effect of age, feeding status and possible role of growth hormone in the process of adipogenesis was also studied. Differences in lipid-filling activity of the tested plasma samples were much more dependent on age than the genotype of plasma donors were. The plasma taken from the oldest (20-week-old) rats stimulated the accumulation of triglycerides in the cells to significantly higher levels than the plasma from other rats. The influence of the feeding status on the lipid-filling activity of plasma was not significant. The differentiation potential of plasma in terms of the stimulation of glycerophosphate dehydrogenase activity measured in adipocyte precursors was 30-50% higher when the culture medium contained plasma from obese rats. Furthermore, glycerophosphate dehydrogenase activity in the growing cells declined with age and tended to be higher in the presence of plasma from fed rats. It was the growth hormone that was in a considerable degree responsible for the differentiation potential of Zucker rat plasma. This effect of growth hormone seemed to be less dependent on fafa genotype. It is, therefore, suggested that in addition to growth hormone, other factors in the plasma of genetically obese Zucker rats might be important in the development of obesity in this rat strain.

Regulation of new fat cell formation.

The formation of new adipocytes occurs either at the stage of multiplication or differentiation or both. It seems possible that the formation of new fat cells is dependent on the average cell weight in a given adipose tissue depot, but there may also be other regional, local regulatory factors. Multiplication of fat cells has been suggested to be stimulated by 17-beta-oestradiol while the differentiation of adipocytes is stimulated by growth hormone, glucocorticoids, insulin, insulin-like growth factor and female sex hormones. There are, probably, other factors acting in circulation or locally. The factors promoting growth of new fat cells with overfeeding are at present unknown. Some hypothetical possibilities are discussed.

Increased DNA synthesis in adipocytes and capillary endothelium in rat adipose tissue during overfeeding.

Adult male rats were subjected to overfeeding with a high-fat, high-sugar diet for 3 and 7 days resulting in a moderate expansion of adipose tissue depots by an increase in fat-cell size. Seventeen hours and 7 days after injection of a pulse of labelled thymidine, specific activity of DNA was examined in different cellular fractions obtained from the epididymal and perirenal adipose tissues after collagenase liberation and separation procedures. A slow increase of formation of new adipocytes occurred after 3 and 7 days of overfeeding, most pronounced in cells from perirenal adipose tissue. Capillary endothelium and cells in the stromal fraction showed a rapid synthesis and turn-over. Overfeeding induced an increased formation of new capillary endothelial cells after 7 days of overfeeding, again most pronounced in perirenal cells. It was concluded that new fat cells are formed at a slow rate early during overfeeding. Capillary endothelium in adipose tissue has a high rate of turnover, and its synthesis is increased further by overfeeding. New adipocytes precede, and possibly stimulate, the formation of new capillaries. Formation of new cells in the remaining stromal-vascular cells is probably occurring at different rates among different types of cells.

Effects of age, obesity and growth-hormone on adipogenic activity in human plasma.

The potential was examined for insulin, growth hormone and insulin-like growth factor (IGF-1) alone or in combinations to stimulate glycerophosphate dehydrogenase (GPDH) activity, a sensitive marker of differentiation of adipose precursor cells in primary culture. Insulin, but not growth hormone or IGF-1, stimulated GPDH in the presence of fetal calf serum and cat serum. The content of growth hormone in adult rat heparinised plasma seemed, however, important for such stimulation, but was also dependent on feeding status of the plasma donor, and was abolished by hypophysectomy of the cell donor. GPDH activity was then analysed in heparinised plasma in the over-night fasting state in humans to examine a potential influence of age, obesity and pregnancy. In comparison with non-obese adults, GPDH-stimulatory activity was higher in plasma from infants and small children. A similar trend was seen in plasma from teenagers. This activity was probably partly dependent on growth hormone, because this increase of activity could be inhibited by excess of anti-human growth hormone antiserum. Obesity in adulthood or among teenagers was not associated with any difference in plasma activity to stimulate cellular differentiation, and plasma from women during late pregnancy had a low stimulating capacity. Simultaneous analyses of the potential of plasma to stimulate lipid accumulation in adipose precursor cells was proportional to the triglyceride concentration. Overall, the inhibitory effect of antihuman growth hormone antiserum on the differentiating capacity of human plasma was small or non-existing. It is therefore suggested that in human plasma, factors other than growth hormone might be important for the differentiation of adipocyte precursor cells.

Adipogenic activity in human plasma. Effects of feeding state and obesity.

The potential of plasma from obese and non-obese subjects to stimulate the formation of new adipocytes was studied by assays in rat adipose precursor cells in primary culture. Adipogenic activity was followed in terms of rate of lipid filling, analysed by determination of triglyceride contents per unit protein, stimulation of multiplication, measured as rate of incorporation of labelled thymidine into DNA, and stimulation of differentiation, followed as an increase in glycerophosphate dehydrogenase activity. Plasma from obese subjects contained an excess of activity stimulating lipid filling, closely associated to the recent body weight histories with increased activity with a recent increase of body weight and vice versa. There was also a strong association with plasma concentration of triglyceride. The importance of the latter was demonstrated by acute feeding experiments with triglyceride, as well as by addition of isolated very-low-density lipoprotein and chylomicron fractions which caused increases of lipid filling activity closely in parallel to triglyceride contents of the culture medium. Specific stimulatory properties of plasma from weight-increasing obese subjects on adipose precursor cell multiplication and differentiation were not found. It was suggested that human obesity with an increased number of adipocytes is not characterized by elevated circulating specific stimulatory factors of new fat cell formation. Such factors are present in excess in both non-obese and obese subjects. It was hypothesized that the elevated lipid filling capacity in obese subjects might modify local inhibitory factors of adipocyte formation.