| 11. |
- Banke, Elin, et al.
(författare)
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Superantigen activates the gp130 receptor on adipocytes resulting in altered adipocyte metabolism.
- 2014
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Ingår i: Metabolism, Clinical and Experimental. - : Elsevier BV. - 1532-8600. ; 63:6, s. 831-840
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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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| 12. |
- Barazzoni, Rocco, et al.
(författare)
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Defining and diagnosing sarcopenia : Is the glass now half full?
- 2023
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Ingår i: Metabolism. - : Elsevier. - 0026-0495 .- 1532-8600. ; 143
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Forskningsöversikt (refereegranskat)abstract
- Low muscle mass and function exert a substantial negative impact on quality of life, health and ultimately survival, but their definition, identification and combination to define sarcopenia have suffered from lack of universal consensus. Methodological issues have also contributed to incomplete agreement, as different approaches, techniques and potential surrogate measures inevitably lead to partly different conclusions. As a consequence: 1) awareness of sarcopenia and implementation of diagnostic procedures in clinical practice have been limited; 2) patient identification and evaluation of therapeutic strategies is largely incomplete. Significant progress has however recently occurred after major diagnostic algorithms have been developed, with common features and promising perspectives for growing consensus. At the same time, the need for further refinement of the sarcopenia concept has emerged, to address its increasingly recognized clinical heterogeneity. This includes potential differential underlying mechanisms and clinical features for age-and disease-driven sarcopenia, and the emerging challenge of sarcopenia in persons with obesity. Here, we will review existing algorithms to diagnose sarcopenia, and major open methodological issues to assess skeletal muscle mass and function under different clinical conditions, in order to highlight similarities and differences. Potential for consensus on sarcopenia diagnosis as well as emerging new challenges will be discussed.
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| 13. |
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| 14. |
- Bauzá-Thorbrügge, Marco, et al.
(författare)
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Adiponectin stimulates Sca1+CD34−-adipocyte precursor cells associated with hyperplastic expansion and beiging of brown and white adipose tissue
- 2024
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Ingår i: Metabolism. - : Elsevier. - 0026-0495 .- 1532-8600. ; 151
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Tidskriftsartikel (refereegranskat)abstract
- Background: The adipocyte hormone adiponectin improves insulin sensitivity and there is an inverse correlation between adiponectin levels and type-2 diabetes risk. Previous research shows that adiponectin remodels the adipose tissue into a more efficient metabolic sink. For instance, mice that overexpress adiponectin show increased capacity for hyperplastic adipose tissue expansion as evident from smaller and metabolically more active white adipocytes. In contrast, the brown adipose tissue (BAT) of these mice looks “whiter” possibly indicating reduced metabolic activity. Here, we aimed to further establish the effect of adiponectin on adipose tissue expansion and adipocyte mitochondrial function as well as to unravel mechanistic aspects in this area. Methods: Brown and white adipose tissues from adiponectin overexpressing (APN tg) mice and littermate wildtype controls, housed at room and cold temperature, were studied by histological, gene/protein expression and flow cytometry analyses. Metabolic and mitochondrial functions were studied by radiotracers and Seahorse-based technology. In addition, mitochondrial function was assessed in cultured adiponectin deficient adipocytes from APN knockout and heterozygote mice. Results: APN tg BAT displayed increased proliferation prenatally leading to enlarged BAT. Postnatally, APN tg BAT turned whiter than control BAT, confirming previous reports. Furthermore, elevated adiponectin augmented the sympathetic innervation/activation within adipose tissue. APN tg BAT displayed reduced metabolic activity and reduced mitochondrial oxygen consumption rate (OCR). In contrast, APN tg inguinal white adipose tissue (IWAT) displayed enhanced metabolic activity. These metabolic differences between genotypes were apparent also in cultured adipocytes differentiated from BAT and IWAT stroma vascular fraction, and the OCR was reduced in both brown and white APN heterozygote adipocytes. In both APN tg BAT and IWAT, the mesenchymal stem cell-related genes were upregulated along with an increased abundance of Lineage−Sca1+CD34− “beige-like” adipocyte precursor cells. In vitro, the adiponectin receptor agonist Adiporon increased the expression of the proliferation marker Pcna and decreased the expression of Cd34 in Sca1+ mesenchymal stem cells. Conclusions: We propose that the seemingly opposite effect of adiponectin on BAT and IWAT is mediated by a common mechanism; while reduced adiponectin levels are linked to lower adipocyte OCR, elevated adiponectin levels stimulate expansion of adipocyte precursor cells that produce adipocytes with intrinsically higher metabolic rate than classical white but lower metabolic rate than classical brown adipocytes. Moreover, adiponectin can modify the adipocytes' metabolic activity directly and by enhancing the sympathetic innervation within a fat depot.
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| 15. |
- Behre, Carl Johan, 1968, et al.
(författare)
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Dissociation between adipose tissue expression and serum levels of adiponectin during and after diet-induced weight loss in obese subjects with and without the metabolic syndrome
- 2007
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Ingår i: Metabolism: Clinical and Experimental. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 56:8, s. 1022-8
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Tidskriftsartikel (refereegranskat)abstract
- The study aimed to examine if dysmetabolic subjects (MetS+) have lower adiponectin gene expression and lower circulating adiponectin levels than non-dysmetabolic obese subjects (MetS-) at baseline, if adiponectin expression and adiponectin concentration rise more in the dysmetabolic group during weight loss, and if v-SNARE Vti1a (vesicle transport soluble NSF attachment protein receptor vps10p tail interacting 1a) expression increases during the weight loss, as a mechanism for increased adiponectin secretion. Twenty-one obese MetS+ and 19 obese MetS- subjects underwent a very low-energy diet for 16 weeks followed by 2 weeks of refeeding. Abdominal subcutaneous adipose tissue biopsies and blood samples were taken before, during, and after dieting for DNA microarray, reverse transcriptase-polymerase chain reaction, and biochemical analyses. Serum adiponectin was also assessed in a sex- and age-matched healthy, nonobese reference group. Weight decreased by 26.3+/-9.8 kg in the MetS+ group and 28.2+/-8.4 kg in the MetS- group with concomitant reductions in insulin, hemoglobin A1c, and triglycerides that were more pronounced in the MetS+ group. Initially, the MetS+ subjects had lower serum adiponectin, but the differences disappeared at week 8, with a continuous increase in serum adiponectin throughout the study in both groups to a level that was higher than in the reference group. The expression of adiponectin and v-SNARE Vti1a did not differ between the groups or over time. In conclusion, obese subjects with the metabolic syndrome had lower circulating adiponectin than subjects without the syndrome. Weight loss increased serum levels of adiponectin without a parallel increase in adiponectin gene expression. The mechanisms involved in the regulation of adiponectin levels merits further investigation.
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| 16. |
- Behre, Carl Johan, 1968, et al.
(författare)
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Serum adiponectin in a population sample of 64-year-old women in relation to glucose tolerance, family history of diabetes, autoimmunity, insulin sensitivity, C-peptide, and inflammation
- 2006
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Ingår i: Metabolism: Clinical and Experimental. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 55:2, s. 188-94
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the study was to describe serum adiponectin levels in a population-based sample of women with different degrees of glucose tolerance and to examine if the variability in serum adiponectin was explained by family history of diabetes, obesity, insulin resistance, glycemia, and inflammation. Repeated oral glucose tolerance tests were used in a screening procedure of a cohort of 64-year-old women to identify those with diabetes mellitus n = 210) and impaired glucose tolerance (n = 201). A random sample of women with normal glucose tolerance (NGT, n = 186) was also included. The examination included history of first-degree relatives with diabetes, anthropometry, measurement of circulating adiponectin, glutamic acid decarboxylase antibodies, blood glucose, HbA1c, insulin, proinsulin, C-peptide, high-sensitivity C-reactive protein, and homeostasis model assessment. Serum adiponectin concentration was lowest among diabetic women, highest in the random-sample NGT group, and intermediate in the impaired glucose tolerance group. This difference was partly explained by homeostasis model assessment, C-peptide, family history, and high-sensitivity C-reactive protein (R2 = 0.33, P < .001), but obesity and glycemia did not contribute to this variability in serum adiponectin. A family history of diabetes was associated with low serum adiponectin concentration independently of obesity, glycemia, or insulin sensitivity (P = .002). Glutamic acid decarboxylase-positive diabetic women (n = 17) had similar serum adiponectin as the NGT group in spite of hyperglycemia. In conclusion, serum adiponectin was lowered in women with type 2 diabetes mellitus, and this difference could only be partly explained by insulin resistance, insulin secretion, family history of diabetes, and inflammation. Family history of diabetes was independently associated with hypoadiponectinemia. Autoimmune diabetic women did not have low adiponectin levels.
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| 17. |
- Bengtsson, Inger M., 1944, et al.
(författare)
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The cortisol awakening response and the metabolic syndrome in a population-based sample of middle-aged men and women.
- 2010
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Ingår i: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 59:7, s. 1012-9
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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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| 18. |
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| 19. |
- Berts, Alf, et al.
(författare)
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Oscillatory Ca2+ signaling in somatostatin-producing cells from the human pancreas
- 1997
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Ingår i: Metabolism. - 0026-0495 .- 1532-8600. ; 46:4, s. 366-369
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Tidskriftsartikel (refereegranskat)abstract
- Oscillatory Ca2+ signaling was studied in human somatostatin-releasing pancreatic δ cells identified by immunostaining. A ratiometric fura-2 technique was used for measuring cytoplasmic concentrations of Ca2+ and Sr2+ in δ cells exposed to the respective cation. Rhythmic activity in terms of slow (frequency, 0.1 to 0.4 per minute) oscillations from close to the basal level was seen in the presence of 3 to 20 mmol/L glucose during superfusion with medium containing 2.6 to 5 mmol/L Ca2+ or 5 mmol/L Sr2. These oscillations could be transformed into a sustained increase by decreasing extracellular Ca2+ or adding 1 mmol/L tolbutamide or 20 nmol/L glucagon. Addition of glucagon to a medium containing 20 mmol/L glucose resulted in the generation of short (< 30 seconds) transients, which disappeared upon exposure to 100 nmol/L of the intracellular Ca2+-adenosine triphosphatase (ATPase) inhibitor thapsigargin. When analyzing small aggregates of islet cells, it became evident that oscillatory activity in δ cells can be synchronous with that in adjacent non—δ cells. It is concluded that secretion of pancreatic somatostatin in man involves Ca2+ signaling similar to that regulating the pulsatile release of insulin.
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| 20. |
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