| 351. |
- Vessby, Bengt, et al.
(författare)
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Plasma lipid fatty acid composition, desaturase activities and insulin sensitivity in Amerindian women
- 2012
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Ingår i: NMCD. Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 22:3, s. 176-181
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Two Amerindian populations - Shuar women living in the Amazonian rain forest under traditional conditions and urbanized women in a suburb of Lima were studied. The fatty acid composition in plasma lipids and the relationships between fatty acid composition and metabolic variables were studied, as well as in a reference group of Swedish women.METHODS AND RESULTS: Fasting plasma was used for analyses of glucose, insulin, leptin and fatty acid composition. Women in Lima had more body fat, higher fasting insulin and leptin and lower insulin sensitivity than the Shuar women, who had insulin sensitivity similar to Swedish women. Shuar women had very high proportions (mean; SD) of palmitoleic (13.2; 3.9%) and oleic (33.9; 3.7%) acids in the plasma cholesteryl esters with very low levels of linoleic acid (29.1; 6.1 3%), as expected on a low fat, high carbohydrate diet. The estimated activity of delta 9 (SCD-1) desaturase was about twice as high in the Shuar compared with Lima women, suggesting neo lipogenesis, while the delta 5 desaturase activity did not differ. The Lima women, as well as the Swedish, showed strong positive correlations between SCD-1 activity on the one hand and fasting insulin and HOMA index on the other. These associations were absent in the Shuar women.CONCLUSIONS: The high SCD-1 activity in the Shuar women may reflect increased lipogenesis in adipose tissue. It also illustrates how a low fat diet rich in non-refined carbohydrates can be linked to a good metabolic situation.
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| 352. |
- Vikman, Jenny, et al.
(författare)
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Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets.
- 2009
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Ingår i: Diabetes, Obesity and Metabolism. - : Wiley. - 1462-8902 .- 1463-1326. ; 11 Suppl 4, s. 197-201
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Tidskriftsartikel (refereegranskat)abstract
- Islet hormone secretion is regulated by a variety of factors, and many of these signal through G protein-coupled receptors (GPCRs). A novel islet GPCR is GPR54, which couples to the Gq isoform of G proteins, which in turn signal through the phospholipase C pathway. Ligands for GPR54 are kisspeptins, which are peptides encoded in the KISS1 gene and also expressed in islet beta-cells. The KISS1 gene encodes a hydrophobic 145-amino acid protein that is cleaved into a 54-amino acid protein, kisspeptin-54 or KP54. Shorter kisspeptins also exist, such as kisspeptin-10 (KP10) and kisspeptin-13 (KP13). The involvement of GPR54 and kisspeptins in the regulation of islet function is not known. To address this problem, we incubated isolated mouse islets in the presence of KP13 and KP54 for 60 min and measured insulin secretion. We found that both KP13 and KP54 at 10 nM, 100 nM and 1microM inhibited insulin secretion in the presence of 2.8 mM glucose. However, by increasing the glucose concentration, this inhibitory action of the kisspeptins vanished. Thus, at 11.1 mM glucose, KP13 and KP54 inhibited insulin secretion only at high doses, and at 16.7 mM they no longer inhibited insulin secretion in any of the doses. We conclude that kisspeptins inhibit insulin secretion at glucose concentrations below 11.1 mM. This suggests that kisspeptins are regulating insulin secretion at physiological concentrations of glucose. The mechanisms by which kisspeptins regulate islet function and insulin secretion are unknown and will be further investigated.
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| 353. |
- Wallenius, Ville, 1970, et al.
(författare)
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Interleukin-6-deficient mice develop mature-onset obesity.
- 2002
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Ingår i: Nature medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 8:1, s. 75-9
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Tidskriftsartikel (refereegranskat)abstract
- The immune-modulating cytokine interleukin-6 (IL-6) is expressed both in adipose tissue and centrally in hypothalamic nuclei that regulate body composition. We investigated the impact of loss of IL-6 on body composition in mice lacking the gene encoding IL-6 (Il6-/- mice) and found that they developed mature-onset obesity that was partly reversed by IL-6 replacement. The obese Il6-/- mice had disturbed carbohydrate and lipid metabolism, increased leptin levels and decreased responsiveness to leptin treatment. To investigate the possible mechanism and site of action of the anti-obesity effect of IL-6, we injected rats centrally and peripherally with IL-6 at low doses. Intracerebroventricular, but not intraperitoneal IL-6 treatment increased energy expenditure. In conclusion, centrally acting IL-6 exerts anti-obesity effects in rodents.
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| 354. |
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| 355. |
- Westergren, Rickard, 1974, et al.
(författare)
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Overexpression of Foxf2 in adipose tissue is associated with lower levels of IRS1 and decreased glucose uptake in vivo.
- 2010
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Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 298:3, s. E548-54
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Tidskriftsartikel (refereegranskat)abstract
- Many members of the forkhead genes family of transcription factors have been implicated as important regulators of metabolism, in particular, glucose homeostasis, e.g., Foxo1, Foxa3, and Foxc2. The purpose of this study was to exploit the possibility that yet unknown members of this gene family play a role in regulating glucose tolerance in adipocytes. We identified Foxf2 in a screen for adipose-expressed forkhead genes. In vivo overexpression of Foxf2 in an adipose tissue-restricted fashion demonstrated that such mice display a significantly induced insulin secretion in response to an intravenous glucose load compared with wild-type littermates. In response to increased Foxf2 expression, insulin receptor substrate 1 (IRS1) mRNA and protein levels are significantly downregulated in adipocytes; however, the ratio of serine vs. tyrosine phosphorylation of IRS1 seems to remain unaffected. Furthermore, adipocytes overexpressing Foxf2 have a significantly lower insulin-mediated glucose uptake compared with wild-type adipocytes. These findings argue that Foxf2 is a previously unrecognized regulator of cellular and systemic whole body glucose tolerance, at least in part, due to lower levels of IRS1. Foxf2 and its downstream target genes can provide new insights with regard to identification of novel therapeutic targets.
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| 356. |
- Westling, Sofie, et al.
(författare)
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Altered glucose tolerance in women with deliberate self-harm
- 2009
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Ingår i: Psychoneuroendocrinology. - : Science direct. - 0306-4530 .- 1873-3360. ; 36:6, s. 878-883
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Tidskriftsartikel (refereegranskat)abstract
- Disturbances in glucose metabolism are of importance for violent behaviour in men, but studies in women are lacking. We used the 5 h-oral glucose tolerance test (OGTT) in this study of 17 female psychiatric patients, selected for violent behaviour directed against themselves (deliberate self-harm) and 17 healthy controls matched for age and BMI. Following OGTT, patients had higher glucose levels at 30 min (p = 0.007) and increased glucagon area under the curve (p = 0.011). Since a co-morbid eating disorder might affect results, we as a post-hoc analysis subgrouped the patients and found that the increased glucagon levels only were present in patients with an eating disorder. In contrast, those without an eating disorder showed a significantly lower p-glucose nadir (p = 0.015) and unaltered glucagon levels compared to controls. There were no significant differences in insulin and C-peptide levels between patients and controls. We conclude that deliberate self-harm in women may be associated with alterations in carbohydrate metabolism in certain groups. Eating disorder is a confounding factor.
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| 357. |
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| 358. |
- Westling, Sofie, et al.
(författare)
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Increased IL-1 beta reactivity upon a glucose challenge in patients with deliberate self-harm
- 2011
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Ingår i: Acta Psychiatrica Scandinavica. - : Wiley. - 1600-0447 .- 0001-690X. ; 124:4, s. 301-306
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Tidskriftsartikel (refereegranskat)abstract
- Objective: A disturbed glucose metabolism has been observed in patients with aggressive behaviour. Interleukin (IL)-1β is a pro-inflammatory cytokine that can induce hypoglycaemia, but has also been suggested to be involved in the generation of hostility and aggression. Our group has previously shown an altered glucose metabolism in patients with self-inflicted aggressive behaviour. We investigated the hypothesis that the levels of IL-1 would be increased in these patients, because this might explain the aberrant glucose metabolism and add further knowledge to the aetiology of self-inflicted aggressive behaviour. Method: We investigated plasma cytokine changes in 13 patients with borderline personality disorder and 13 healthy controls during a 5-h glucose challenge. Plasma samples were analysed for cytokines IL-1β, TNF-α and IL-6 using high-sensitivity multiplex ELISA. Psychiatric symptoms were rated using the Aggression Questionnaire Revised Swedish Version. Results: Basal plasma levels of the three cytokines did not differ between patients and controls. All three cytokines reacted significantly upon the glucose challenge. The increase in IL-1β levels in response to glucose was significantly greater in patients than in controls. Furthermore, IL-1β reactivity was associated with symptoms of hostility. Conclusion: An increased reactivity of IL-1β might be part of a pathogenetic mechanism in patients with deliberate self-harm.
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| 359. |
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| 360. |
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