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Sökning: L773:0026 0495 > (2010-2014)

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2.
  • Bah Rösman, Jessica, 1975, et al. (författare)
  • Further exploration of the possible influence of polymorphisms in HTR2C and 5HTT on body weight.
  • 2010
  • Ingår i: Metabolism. - : Elsevier BV. - 0026-0495. ; 59:8, s. 1156-1163
  • Tidskriftsartikel (refereegranskat)abstract
    • Receptors of the 5-HT2C subtype are of importance for the influence of serotonin on food intake, and 2 single nucleotide polymorphisms in this gene (HTR2C)-Cys23Ser (rs6318) and -759C>T (rs3813929)-have been reported to be associated with weight and/or antipsychotic-induced weight gain. The present study aimed to replicate these associations; in addition, the 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene (SLC6A4) was assessed. The polymorphisms were genotyped in subjects recruited from the normal population (n = 510), and possible associations between genotype and body mass index (BMI) were assessed. The Ser23 allele was more common in underweight subjects (BMI <20) than in normal- and overweight (BMI >/=20) subjects (P = .006). The T allele of the -759C/T polymorphism was less common in the overweight group (BMI >/=25) (P = .007). Homozygosity for the short allele of 5-HTTLPR was more frequent in underweight subjects (P = .015). Our results are in agreement with previous studies, suggesting polymorphisms in HTR2C to be associated with body weight, particularly in women; and they also suggest that 5-HTTLPR may influence this phenotype. Further studies on the importance of the investigated genes for eating disorders and drug-induced weight gain are warranted.
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3.
  • Banke, Elin, et al. (författare)
  • Superantigen activates the gp130 receptor on adipocytes resulting in altered adipocyte metabolism.
  • 2014
  • Ingår i: Metabolism, Clinical and Experimental. - : Elsevier BV. - 1532-8600. ; 63:6, s. 831-840
  • Tidskriftsartikel (refereegranskat)abstract
    • The bacteria Staphylococcus aureus is part of the normal bacterial flora and produces a repertoire of enterotoxins which can cause food poisoning and toxic shock and might contribute to the pathogenesis of inflammatory diseases. These enterotoxins directly cross-link the T cell receptor with MHC class II, activating large amounts of T cells and are therefore called superantigens. It was recently discovered that the superantigen SEA binds to the cytokine receptor gp130. As obesity and type 2 diabetes are highly associated with inflammation of the adipose tissue and gp130 has been shown to play an important role in adipocytes, we wanted to investigate the effect of SEA on adipocyte signaling and function.
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5.
  • Bengtsson, Inger M., 1944, et al. (författare)
  • The cortisol awakening response and the metabolic syndrome in a population-based sample of middle-aged men and women.
  • 2010
  • Ingår i: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 59:7, s. 1012-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective was to explore the relationship between the cortisol awakening response (CAR) and the metabolic syndrome (MetS) as defined by the National Cholesterol Education Program criteria. The final study sample consisted of 91 women (14 with MetS) and 84 men (15 with MetS), aged 45 to 70 years, from a general population sample. The only exclusion criteria were no consent, pregnancy, or insufficient cortisol testing. On the day of measurement (weekday), salivary cortisol was sampled at awakening and 15 minutes after awakening. Relative CAR (CAR%) and the MetS were the main variables studied. Results showed that, in women with the MetS, cortisol at awakening was significantly lower (mean, 8.92 vs 12.33 nmol/L; P = .05) and the CAR was significantly higher (91.4% vs 36.5%, P < .001) than in women without the syndrome. Significant difference in the relative CAR was also present between men and women with MetS (38.5% and 91.4%, respectively; P = .02). No difference was seen in the awakening response comparing men with and without the MetS. In a regression model, the response to awakening was dependent on the MetS in women (F1,89 = 13.19, P < .001); but the model was not significant in men. Furthermore, the awakening response was associated with more depressive symptoms in women (F1,80 = 8.12, P = .01) and with weekday/weekend cortisol sampling in men (F1,82 = 4.63, P = .03). The association between the relative CAR and the MetS remained significant but somewhat attenuated after adjusting for depressive symptoms (P = .01). Results indicate a sex difference in the CAR% in the presence of the MetS independent of depressive symptoms, a known correlate of the MetS.
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7.
  • Garrido, Pablo, et al. (författare)
  • Negative regulation of glucose metabolism in human myotubes by supraphysiological doses of 17 beta-estradiol or testosterone
  • 2014
  • Ingår i: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 63:9, s. 1178-1187
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. Exposure of skeletal muscle to high levels of testosterone or estrogen induces insulin resistance, but evidence regarding the direct role of either sex hormone on metabolism is limited. Therefore, the aim of this study was to investigate the direct effect of acute sex hormone exposure on glucose metabolism in skeletal muscle. Materials/Methods. Differentiated human skeletal myotubes were exposed to either 17 beta-estradiol or testosterone and metabolic characteristics were assessed. Glucose incorporation into glycogen, glucose oxidation, palmitate oxidation, and phosphorylation of key signaling proteins were determined. Results. Treatment of myotubes with either 17 beta-estradiol or testosterone decreased glucose incorporation into glycogen. Exposure of myotubes to 17 beta-estradiol reduced glucose oxidation under basal and insulin-stimulated conditions. However, testosterone treatment enhanced basal palmitate oxidation and prevented insulin action on glucose and palmitate oxidation. Acute stimulation of myotubes with testosterone reduced phosphorylation of S6K1 and p38 MAPK. Exposure of myotubes to either 17 beta-estradiol or testosterone augmented phosphorylation GSK3 beta(ser9) and PKC delta(Thr505), two negative regulators of glycogen synthesis. Treatment of myotubes with a PKC specific inhibitor (GFX) restored the effect of either sex hormone on glycogen synthesis. PKC delta silencing restored glucose incorporation into glycogen to baseline in response to 17 beta-estradiol, but not testosterone treatment. Conclusion. An acute exposure to supraphysiological doses of either 17 beta-estradiol or testosterone regulates glucose metabolism, possibly via PKC signaling pathways. Furthermore, testosterone treatment elicits additional alterations in serine/threonine kinase signaling, including the ribosomal protein S6K1 and p38 MAPK.
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8.
  • Goedecke, Julia H, et al. (författare)
  • Ethnic differences in serum lipoproteins and their determinants in South African women
  • 2010
  • Ingår i: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 59:9, s. 1341-1350
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective of the study was to characterize ethnic differences in lipid levels and low-density lipoprotein (LDL) particle size and subclasses in black and white South African women and to explore the associations with insulin sensitivity (S(I)), body composition, and lifestyle factors. Fasting serum lipids and LDL size and subclasses, body composition (dual-energy x-ray absorptiometry), and S(I) (frequently sampled intravenous glucose tolerance test) were measured in normal-weight (body mass index <25 kg/m(2)) black (n = 15) and white (n = 15), and obese (body mass index >30 kg/m(2)) black (n = 13) and white (n = 13) women. Normal-weight and obese black women had lower triglycerides (0.59 +/- 0.09 and 0.77 +/- 0.10 vs 0.89 +/- 0.09 and 0.93 +/- 0.10 mmol/L, P < .05) and high-density lipoprotein cholesterol (1.2 +/- 0.1 and 1.1 +/- 0.1 vs 1.7 +/- 0.1 and 1.6 +/- 0.3 mmol/L, P < .01) than white women. The LDL particle size was not different, but obese black women had more LDL subclass IV (17.3% +/- 1.0% vs 12.5% +/- 1.0%, P < .01). In white women, triglycerides and LDL particle size correlated with S(I) (P < .01), whereas cholesterol levels correlated with body fat (P < .05). Low socioeconomic status, low dietary protein intake, and injectable contraceptive use were the major determinants of unfavorable lipid profiles in black women. Black women had lower triglyceride and high-density lipoprotein cholesterol levels and more small dense LDL particles than white women. The major determinants of serum lipids in black women were socioeconomic status and lifestyle factors, whereas in white women, S(I) and body composition most closely correlated with serum lipids.
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10.
  • Jans, A., et al. (författare)
  • Impact of dietary fat quantity and quality on skeletal muscle fatty acid metabolism in subjects with the metabolic syndrome
  • 2012
  • Ingår i: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 61:11, s. 1554-1565
  • Tidskriftsartikel (refereegranskat)abstract
    • Insulin resistance is characterized by disturbances in lipid metabolism in skeletal muscle. Our aim was to investigate whether gene expression and fatty acid (FA) profile of skeletal muscle lipids are affected by diets differing in fat quantity and quality in subjects with the metabolic syndrome (MetS) and varying degrees of insulin sensitivity. 84 subjects (age 57.3 ± 0.9 y, BMI 30.9 ± 0.4 kg/m 2, 42 M/42 F) were randomly assigned to one of four iso-energetic diets: high-SFA (HSFA); high-MUFA (HMUFA) or two low-fat, high-complex carbohydrate diets, supplemented with 1.24 g/day of long-chain n-3 PUFA (LFHCCn-3) or control oil (LFHCC) for 12 weeks. In a subgroup of men (n = 26), muscle TAG, DAG, FFA and phospholipid contents were determined including their fractional synthetic rate (FSR) and FA composition at fasting and 4 h after consumption of a high-fat mixed-meal, both pre- and post-intervention. Genes involved in lipogenesis were downregulated after HMUFA (mean fold change - 1.3) and after LFHCCn-3 (fold change - 1.7) in insulin resistant subjects (< median of (S I)), whereas in insulin sensitive subjects (> median of insulin sensitivity) the opposite effect was shown (fold change + 1.6 for both diets). HMUFA diet tended to decrease FSR in TAG (P =.055) and DAG (P =.066), whereas the LFHCCn-3 diet reduced TAG content (P =.032). In conclusion, HMUFA and LFHCCn-3 diets reduced the expression of the lipogenic genes in skeletal muscle of insulin resistant subjects, whilst HMUFA reduced the fractional synthesis rate of DAG and TAG and LFHCC n-3 the TAG content. Our data indicate that these diets may reduce muscle fat accumulation by affecting the balance between FA synthesis, storage and oxidation.
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