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Sökning: LAR1:lu > Ahrén Bo

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1.
  • 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 Verlag. - 0012-186X. ; 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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3.
  • Borch, Kurt, et al. (författare)
  • Gastric carcinoids: biologic behavior and prognosis after differentiated treatment in relation to type
  • 2005
  • Ingår i: Annals of surgery. - 0003-4932 (Print). ; 242:1, s. 64-73
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To analyze tumor biology and the outcome of differentiated treatment in relation to tumor subtype in patients with gastric carcinoid. Background: Gastric carcinoids may be subdivided into ECL cell carcinoids (type 1 associated with atrophic gastritis, type 2 associated with gastrinoma, type 3 without predisposing conditions) and miscellaneous types (type 4). The biologic behavior and prognosis vary considerably in relation to type. Methods: A total of 65 patients from 24 hospitals (51 type 1, 1 type 2, 4 type 3, and 9 type 4) were included. Management recommendations were issued for newly diagnosed cases, that is, endoscopic or surgical treatment of type 1 and 2 carcinoids (including antrectomy to abolish hypergastrinemia) and radical resection for type 3 and 4 carcinoids. Results: Infiltration beyond the submucosa occurred in 9 of 51 type 1, 4 of 4 type 3, and 7 of 9 type 4 carcinoids. Metastases occurred in 4 of 51 type 1 (3 regional lymph nodes, 1 liver), the single type 2 (regional lymph nodes), 3 of 4 type 3 (all liver), and 7 of 9 type 4 carcinoids (all liver). Of the patients with type 1 carcinoid, 3 had no specific treatment, 40 were treated with endoscopic or surgical excision (in 10 cases combined with antrectomy), 7 underwent total gastrectomy, and 1 underwent proximal gastric resection. Radical tumor removal was not possible in 2 of 4 patients with type 3 and 7 of 9 patients with type 4 carcinoid. Five- and 10-year crude survival rates were 96.1% and 73.9% for type 1 (not different from the general population), but only 33.3% and 22.2% for type 4 carcinoids. Conclusion: Subtyping of gastric carcinoids is helpful in the prediction of malignant potential and long-term survival and is a guide to management. Long-term survival did not differ from that of the general population regarding type 1 carcinoids but was poor regarding type 4 carcinoids. Copyright © 2005 by Lippincott Williams & Wilkins.
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4.
  • Otten, Julia, et al. (författare)
  • Surrogate measures of insulin sensitivity vs the hyperinsulinaemic-euglycaemic clamp: a meta-analysis
  • 2014
  • Ingår i: Diabetologia. - Springer Verlag. - 1432-0428. ; 57:9, s. 1781-1788
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis We aimed to identify which surrogate index of insulin sensitivity has the strongest correlation with the reference measurement, the hyperinsulinaemic-euglycaemic clamp (HEC), to determine which surrogate measure should be recommended for use in large-scale studies. Methods A literature search (1979-2012) was conducted to retrieve all articles reporting bivariate correlations between the HEC and surrogate measures of insulin sensitivity (in fasting samples or during the OGTT). We performed a random effects meta-analysis for each surrogate measure to integrate the correlation coefficients of the different studies. Results The OGTT-based surrogate measures with the strongest pooled correlations (r) to the HEC were the Stumvoll metabolic clearance rate (Stumvoll MCR; r=0.70 [95% CI 0.61, 0.77], n=5), oral glucose insulin sensitivity (OGIS; r=0.70 [0.57, 0.80], n=6), the Matsuda index (r=0.67 [0.61, 0.73], n=19), the Stumvoll insulin sensitivity index (Stumvoll ISI; r=0.67 [0.60, 0.72], n=8) and the Gutt index (r=0.65 [0.60, 0.69], n=6). The fasting surrogate indices that correlated most strongly with the HEC and had narrow 95% CIs were the revised QUICKI (r=0.68 [0.58, 0.77], n=7), the QUICKI (r=0.61 [0.55, 0.65], n=35), the log HOMA-IR (r=-0.60 [-0.66, -0.53], n=22) and the computer generated HOMA of insulin sensitivity (HOMA-%S; r=0.57 [0.46, 0.67], n=5). Conclusions/interpretation The revised QUICKI fasting surrogate measure appears to be as good as the OGTT-based Stumvoll MCR, OGIS, Matsuda, Stumvoll ISI and Gutt indices for estimating insulin sensitivity. It can therefore be recommended as the most appropriate index for use in large-scale clinical studies.
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6.
  • 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.
  • 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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10.
  • Agardh, Carl-David, et al. (författare)
  • Long-standing hyperglycemia in C57BL/6J mice does not affect retinal glutathione levels or endothelial/pericyte ratio in retinal capillaries
  • 2000
  • Ingår i: Journal of Diabetes and its Complications. - Elsevier. - 1873-460X. ; 14:3, s. 146-153
  • Tidskriftsartikel (refereegranskat)abstract
    • Free radicals have been suggested to play a role in the development of diabetic retinopathy. The aim of the present study was to examine whether the metabolic perturbations caused by high-fat feeding of two strains of mice, the C57BL6/J mice and the NMRI mice, interfere with one of the free radical enzyme defense systems in the retina, i. e., glutathione (GSH), and whether morphological changes occur in the retinal vessels. C57BL/6J mice and NMRI mice were fed a high-fat diet (55%) for 18 months. High-fat fed mice of both strains developed overweight, hyperinsulinemia, and hyperlipidemia. In addition, the high-fat fed C57BL/6J mice also developed sustained hyperglycemia for at least 15 months. The C57BL/6J mice had lower retinal GSH levels than the NMRI mice, both when given a normal diet (29.6+/-1.2 vs. 37.1+/-1.4 nmol/mg protein; p<0.01) and when given a high-fat diet (27.0+/-1.6 vs. 34.7+/-2.6 nmol/mg protein; p<0.05). Despite the long-standing hyperglycemia, hyperinsulinemia and hyperlipidemia in the C57BL/6J mice, high-fat feeding did not cause any changes in the retinal tissue levels of GSH (27.0+/-1.6 vs. 29. 6+/-1.2 nmol/mg protein) or cysteine (7.61+/-0.63 vs. 6.80+/-0.59 nmol/mg protein). Similarly, high-fat feeding did not affect retinal GSH or cysteine levels in NMRI mice. No light microscopical retinal vessel changes were seen, either in C57BL/6J or in NMRI mice. The study therefore shows that long-standing metabolic perturbations induced by dietary obesity do not induce signs of retinopathy in two different strains of mice. Further studies are needed to explore whether this is explained by increased expression of protecting systems making these strains of mice resistant to effects of oxidative stress.
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