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1.
  • Ahren, Jonatan, et al. (författare)
  • Increased beta-cell volume in mice fed a high-fat diet A dynamic study over 12 months
  • 2010
  • Ingår i: Islets. - : Landes Bioscience. - 1938-2022. ; 2:6, s. 353-356
  • Tidskriftsartikel (refereegranskat)abstract
    • As we previously demonstrated, there is an adaptive increase in insulin secretion in insulin resistance in the model of high-fat fed female mice. Since it is assumed that islets also adapt to insulin resistance with beta-cell expansion, we have now examined beta-cell volume in this experimental model. Female C57BL/6JBomTac mice were therefore fed a high-fat diet (60% fat from lard) for three, six or twelve months and beta-cell volume was estimated as beta-cell area per islet, individual beta-cell size and beta-cell number per islet. Control animals were fed a normal chow (11% fat). We found that beta-cell area per islet and total number of beta-cells per islet were increased already after three months of high-fat feeding and that this increase was sustained throughout the twelve month study period. In contrast, individual beta-cell size showed a dynamic pattern with a reduction after three months followed by increase after six and twelve months. The number of apoptosis (caspase-3) positive beta-cells was reduced after three months, whereas there was no difference in proliferation (Ki-67) positive cells, although these were generally rarely observed. Thus, we conclude that insulin resistance accompanying high-fat feeding in mice is followed by progressive beta-cell expansion as evident by early increased islet beta-cell volume and total number of beta-cells, whereas individual beta-cell size showed a dynamic response. The model is also associated with an early reduced apoptosis, which may contribute to the increased beta-cell volume.
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3.
  • Dencker, Magnus, et al. (författare)
  • Body fat related to daily physical activity and insulin concentrations in non-diabetic children.
  • 2008
  • Ingår i: Clinical Physiology and Functional Imaging. - : John Wiley & Sons Inc.. - 1475-0961. ; 28, s. 211-215
  • Tidskriftsartikel (refereegranskat)abstract
    • This study explored the associations between body fat versus daily physical activity and insulin concentrations in non-diabetic young children in a cross-sectional study of 172 children (93 boys and 79 girls) aged 8-11 years. Blood samples were analysed for serum insulin and daily physical activity was measured by accelerometers. Time spent performing vigorous activity was estimated from accelerometer data by using established cut-off points. Dual-energy x-ray absorptiometry (DXA) was used to quantify abdominal fat mass (AFM) and total body fat (TBF), also calculated as percentage of body weight (BF%). Body fat distribution was calculated as AFM/TBF. Body fat distribution was independently linked to both insulin concentrations and physical activity. In contrast, TBF, AFM, and BF% were linked to physical activity only and not to insulin concentrations. In conclusion in this population of non-diabetic children, body fat distribution was independently associated with increased concentrations of insulin and deceased amount of vigorous activity per day. Also, AFM, TBF, and BF% were independently related to minutes of vigorous activity per day.
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4.
  • Pacini, Giovanni, et al. (författare)
  • Reappraisal of the intravenous glucose tolerance index for a simple assessment of insulin sensitivity in mice
  • 2009
  • Ingår i: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119. ; 296:5, s. 1316-1324
  • Tidskriftsartikel (refereegranskat)abstract
    • Pacini G, Ahren M, Ahren B. Reappraisal of the intravenous glucose tolerance index for a simple assessment of insulin sensitivity in mice. Am J Physiol Regul Integr Comp Physiol 296: R1316-R1324, 2009. First published February 11, 2009; doi: 10.1152/ajpregu.90575.2008.- Mice are increasingly used in studies where measuring insulin sensitivity (IS) is a common procedure. The glucose clamp is labor intensive, cannot be used in large numbers of animals, cannot be repeated in the same mouse, and has been questioned as a valid tool for IS in mice; thus, the minimal model with 50-min intravenous glucose tolerance test (IVGTT) data was adapted for studies in mice. However, specific software and particular ability was needed. The aim of this study was to establish a simple procedure for evaluating IS during IVGTT in mice (CSI). IVGTTs (n = 520) were performed in NMRI and C57BL/6J mice (20-25g). After glucose injection (1 g/kg), seven samples were collected for 50 min for glucose and insulin measurements, analyzed with a minimal model that provided the validated reference IS (S-perpendicular to). By using the regression CS perpendicular to = alpha(1) + alpha(2) x K-G/AUC(D), where K-G is intravenous glucose tolerance index and AUC(D) is the dynamic area under the curve, IS was calculated in 134 control animals randomly selected (regression CSI vs. S-I: r = 0.66, P < 0.0001) and yielded alpha(1) = 1.93 and alpha(2) = 0.24. KG is the slope of log (glucose(5-20)) and AUCD is the mean dynamic area under insulin curve in the IVGTT. By keeping fixed alpha(1) and alpha(2), CSI was validated in 143 control mice (4.7 +/- 0.2 min . mu U- . ml(-1), virtually identical to S-I: 4.7 +/- 0.3, r = 0.89, P < 0.0001); and in 123 mice in different conditions: transgenic, addition of neuropeptides, incretins, and insulin (CSI: 6.0 +/- 0.4 vs. SI: 6.1 +/- 0.4, r = 0.94, P < 0.0001). In the other 120 animals, CSI revealed its ability to segregate different categories, as does S-I. This easily usable formula for calculating CSI overcomes many experimental obstacles and may be a simple alternative to more complex procedures when large numbers of mice or repeated experiments in the same animals are required.
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5.
  • 1666. 1999. 2000. 2020. : Campus Helsingborg 20 år.
  • 2020
  • Samlingsverk (redaktörskap) (populärvet., debatt m.m.)abstract
    • Campus Helsingborg, Lunds universitet firar 20-årsjubileum. Hur gick det till när den gamla Tretornfabriken blev universitet, hur växte utbildning och forskning fram och vart är campus på väg? I denna jubileumsbok tecknas bilder av Campus Helsingborgs tillblivelse, utveckling och framtid. Här möter du några av alla de som formar och format lärosätet. Genom ankedoter, personliga betraktelser och reflektioner ger denna rikt illustrerade bok bred inblick i Helsingborgs campus.
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7.
  • Abdelgadir, M, et al. (författare)
  • Reduced leptin concentrations in subjects with type 2 diabetes mellitus in Sudan.
  • 2002
  • Ingår i: Metabolism, Clinical and Experimental. - : Elsevier. - 1532-8600. ; 51:3, s. 304-306
  • Tidskriftsartikel (refereegranskat)abstract
    • Differences have been observed in the relationship between leptin and metabolic perturbations in glucose homeostasis. Because no information is available from indigenous African populations with diabetes, the purpose of this study was to investigate the possible associations between leptin and different clinical and biochemical characteristics of a large group of subjects with type 2 diabetes mellitus in Sudan. A total of 104 (45 men and 59 women) consecutive type 2 diabetes patients and 75 control subjects (34 men and 41 women) were studied. The body mass index (BMI), blood glucose, serum insulin, and proinsulin were measured and related to serum leptin concentrations. Leptin was higher in females than in males and correlated significantly to BMI. The main novel finding was that serum leptin was significantly lower in diabetic subjects compared with controls in both females (P =.0001) and males (P =.019), although BMI did not differ between diabetic and nondiabetic subjects. Diabetic subjects treated with sulphonylurea (n = 81) had lower BMI than those treated with diet alone or other hypoglycemic drugs (n = 23) (P =.0017), but there was no difference in leptin levels between the 2 groups after adjustment for BMI (P =.87). In diabetic subjects, serum leptin correlated positively with the homeostatic assessment (HOMA) of both beta-cell function (P =.018) and insulin resistance (P =.038), whereas in control subjects, leptin correlated with insulin resistance (P =.0016), but not with beta-cell function. Diabetic subjects had higher proinsulin levels (P =.0031) and higher proinsulin to insulin ratio (P =.0003) than nondiabetic subjects. In univariate analysis, proinsulin showed a weak correlation to leptin (P =.049). In conclusion, we show in a large cohort of Sudanese subjects with type 2 diabetes that circulating leptin levels are lower in diabetic subjectss than in controls of similar age and BMI. The lower serum leptin in diabetic subjects may be a consequence of differences in fat distribution.
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8.
  • Abels, Mia, et al. (författare)
  • CART is overexpressed in human type 2 diabetic islets and inhibits glucagon secretion and increases insulin secretion
  • 2016
  • Ingår i: Diabetologia. - : Springer. - 0012-186X .- 1432-0428. ; 59:9, s. 1928-1937
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis: Insufficient insulin release and hyperglucagonaemia are culprits in type 2 diabetes. Cocaine- and amphetamine-regulated transcript (CART, encoded by Cartpt) affects islet hormone secretion and beta cell survival in vitro in rats, and Cart−/− mice have diminished insulin secretion. We aimed to test if CART is differentially regulated in human type 2 diabetic islets and if CART affects insulin and glucagon secretion in vitro in humans and in vivo in mice. Methods: CART expression was assessed in human type 2 diabetic and non-diabetic control pancreases and rodent models of diabetes. Insulin and glucagon secretion was examined in isolated islets and in vivo in mice. Ca2+ oscillation patterns and exocytosis were studied in mouse islets. Results: We report an important role of CART in human islet function and glucose homeostasis in mice. CART was found to be expressed in human alpha and beta cells and in a subpopulation of mouse beta cells. Notably, CART expression was several fold higher in islets of type 2 diabetic humans and rodents. CART increased insulin secretion in vivo in mice and in human and mouse islets. Furthermore, CART increased beta cell exocytosis, altered the glucose-induced Ca2+ signalling pattern in mouse islets from fast to slow oscillations and improved synchronisation of the oscillations between different islet regions. Finally, CART reduced glucagon secretion in human and mouse islets, as well as in vivo in mice via diminished alpha cell exocytosis. Conclusions/interpretation: We conclude that CART is a regulator of glucose homeostasis and could play an important role in the pathophysiology of type 2 diabetes. Based on the ability of CART to increase insulin secretion and reduce glucagon secretion, CART-based agents could be a therapeutic modality in type 2 diabetes.
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10.
  • Accili, D., et al. (författare)
  • What ails the beta-cell?
  • 2010
  • Ingår i: Diabetes, Obesity and Metabolism. - : Wiley-Blackwell. - 1462-8902. ; 12, s. 1-3
  • Tidskriftsartikel (övrigt vetenskapligt)
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