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1.
  • Abrahamsson, Niclas, et al. (författare)
  • Gastric Bypass Reduces Symptoms and Hormonal Responses in Hypoglycemia
  • 2016
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 65:9, s. 2667-2675
  • Tidskriftsartikel (refereegranskat)abstract
    • Gastric bypass (GBP) surgery, one of the most common bariatric procedures, induces weight loss and metabolic effects. The mechanisms are not fully understood, but reduced food intake and effects on gastrointestinal hormones are thought to contribute. We recently observed that GBP patients have lowered glucose levels and frequent asymptomatic hypoglycemic episodes. Here, we subjected patients before and after undergoing GBP surgery to hypoglycemia and examined symptoms and hormonal and autonomic nerve responses. Twelve obese patients without diabetes (8 women, mean age 43.1 years [SD 10.8] and BMI 40.6 kg/m(2) [SD 3.1]) were examined before and 23 weeks (range 19-25) after GBP surgery with hyperinsulinemic-hypoglycemic clamp (stepwise to plasma glucose 2.7 mmol/L). The mean change in Edinburgh Hypoglycemia Score during clamp was attenuated from 10.7 (6.4) before surgery to 5.2 (4.9) after surgery. There were also marked postsurgery reductions in levels of glucagon, cortisol, and catecholamine and the sympathetic nerve responses to hypoglycemia. In addition, growth hormone displayed a delayed response but to a higher peak level. Levels of glucagon-like peptide 1 and gastric inhibitory polypeptide rose during hypoglycemia but rose less postsurgery compared with presurgery. Thus, GBP surgery causes a resetting of glucose homeostasis, which reduces symptoms and neurohormonal responses to hypoglycemia. Further studies should address the underlying mechanisms as well as their impact on the overall metabolic effects of GBP surgery.
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2.
  • Abrahamsson, Niclas, 1976-, et al. (författare)
  • Gastric bypass reduces symptoms and hormonal responses to hypoglycemia
  • 2016
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 65:9, s. 2667-2675
  • Tidskriftsartikel (refereegranskat)abstract
    • Gastric bypass (GBP) surgery, one of the most common bariatric procedures, induces weight loss and metabolic effects. The mechanisms are not fully understood, but reduced food intake and effects on gastrointestinal hormones are thought to contribute. We recently observed that GBP patients have lowered glucose levels and frequent asymptomatic hypoglycemic episodes. Here, we subjected patients before and after undergoing GBP surgery to hypoglycemia and examined symptoms and hormonal and autonomic nerve responses. Twelve obese patients without diabetes (8 women, mean age 43.1 years [SD 10.8] and BMI 40.6 kg/m(2) [SD 3.1]) were examined before and 23 weeks (range 19-25) after GBP surgery with hyperinsulinemic-hypoglycemic clamp (stepwise to plasma glucose 2.7 mmol/L). The mean change in Edinburgh Hypoglycemia Score during clamp was attenuated from 10.7 (6.4) before surgery to 5.2 (4.9) after surgery. There were also marked postsurgery reductions in levels of glucagon, cortisol, and catecholamine and the sympathetic nerve responses to hypoglycemia. In addition, growth hormone displayed a delayed response but to a higher peak level. Levels of glucagon-like peptide 1 and gastric inhibitory polypeptide rose during hypoglycemia but rose less postsurgery compared with presurgery. Thus, GBP surgery causes a resetting of glucose homeostasis, which reduces symptoms and neurohormonal responses to hypoglycemia. Further studies should address the underlying mechanisms as well as their impact on the overall metabolic effects of GBP surgery.
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4.
  • Ahlqvist, Emma, et al. (författare)
  • A link between GIP and osteopontin in adipose tissue and insulin resistance.
  • 2013
  • Ingår i: Diabetes. - : American Diabetes Association Inc.. - 1939-327X. ; 62:6, s. 2088-2094
  • Tidskriftsartikel (refereegranskat)abstract
    • Low grade inflammation in obesity is associated with accumulation of the macrophagederived cytokine osteopontin in adipose tissue and induction of local as well as systemic insulin resistance. Since GIP (glucose-dependent insulinotropic polypeptide) is a strong stimulator of adipogenesis and may play a role in the development of obesity, we explored whether GIP directly would stimulate osteopontin (OPN) expression in adipose tissue and thereby induce insulin resistance. GIP stimulated OPN protein expression in a dose-dependent fashion in rat primary adipocytes. The level of OPN mRNA was higher in adipose tissue of obese individuals (0.13±}0.04 vs 0.04±}0.01, P<0.05) and correlated inversely with measures of insulin sensitivity (r=-0.24, P=0.001). A common variant of the GIP receptor (GIPR) (rs10423928) gene was associated with lower amount of the exon 9 containing isoform required for transmembrane activity. Carriers of the A-allele with a reduced receptor function showed lower adipose tissue OPN mRNA levels and better insulin sensitivity. Together, these data suggest a role for GIP not only as an incretin hormone, but also as a trigger of inflammation and insulin resistance in adipose tissue. Carriers of GIPR rs10423928 A-allele showed protective properties via reduced GIP effects. Identification of this unprecedented link between GIP and OPN in adipose tissue might open new avenues for therapeutic interventions.
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5.
  • Ahrén, Bo (författare)
  • beta- and alpha-Cell Dysfunction in Subjects Developing Impaired Glucose Tolerance Outcome of a 12-Year Prospective Study in Postmenopausal Caucasian Women
  • 2009
  • Ingår i: Diabetes. - : American Diabetes Association Inc.. - 1939-327X. ; 58:3, s. 726-731
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE-This study assessed insulin and glucagon secretion in relation to insulin sensitivity in Caucasian women who develop impaired glucose tolerance (IGT) versus those who maintain normal glucose tolerance (NGT) over a 12-year period. RESEARCH DESIGN AND METHODS-At baseline and after 3, 8, and 12 years, glucose tolerance (75-g oral glucose tolerance test), insulin sensitivity (euglycemic-hyperinsulinemic clamp), and insulin and glucagon secretion (2- to 5-min responses to 5 g arginine i.v. at fasting, 14 and >25 mmol/l glucose) were determined in 53 healthy Caucasian women (aged 58 years at. baseline) who all had NGT at baseline. RESULTS-During the 12-year period, 26 subjects developed IGT, whereas the remaining 27 subjects maintained NGT throughout the 12-year period. Subjects developing IGT had lower insulin sensitivity than those maintaining NGT in the tests preceding diagnosis of IGT (P <= 0.05). When judged in relation to insulin sensitivity, P-cell glucose sensitivity and maximal insulin secretion were lower in those who later developed IGT than in those maintaining NGT at all tests (P : 0.05). Furthermore, subject's who developed IGT had defective suppression of glucagon secretion by glucose in the test preceding diagnosis of IGT when they still had NGT (P : 0.05). CONCLUSIONS-beta- and alpha-cell dysfunction are evident several years before diagnosis of IGT, and islet dysfunction is manifeste as impaired glucose sensitivity of the beta- and (x-cells and reduced maximal insulin secretion. Diabetes 58:726-731, 2009
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6.
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7.
  • Ahrén, Bo, et al. (författare)
  • Neuropeptides and the regulation of islet function.
  • 2006
  • Ingår i: Diabetes. - : American Diabetes Association Inc.. - 1939-327X. ; 55:Suppl 2, s. 98-107
  • Tidskriftsartikel (refereegranskat)abstract
    • The pancreatic islets are richly innervated by autonomic nerves. The islet parasympathetic nerves emanate from intrapancreatic ganglia, which are controlled by preganglionic vagal nerves. The islet sympathetic nerves are postganglionic with the nerve cell bodies located in ganglia outside the pancreas. The sensory nerves originate from dorsal root ganglia near the spinal cord. Inside the islets, nerve terminals run close to the endocrine cells. In addition to the classic neurotransmitters acetylcholine and norepinephrine, several neuropeptides exist in the islet nerve terminals. These neuropeptides are vasoactive intestinal polypeptide, pituitary adenylate cyclase-activating polypeptide, gastrin-releasing polypeptide, and cocaine-and amphetamine-regulated transcript in parasympathetic nerves; neuropeptide Y and galanin in the sympathetic nerves; and calcitonin gene-related polypeptide in sensory nerves. Activation of the parasympathetic nerves and administration of their neurotransmitters stimulate insulin and glucagon secretion, whereas activation of the sympathetic nerves and administration of their neurotransmitters inhibit insulin but stimulate glucagon secretion. The autonomic nerves contribute to the cephalic phase of insulin secretion, to glucagon secretion during hypoglycemia, to pancreatic polypeptide secretion, and to the inhibition of insulin secretion, which is seen during stress. In rodent models of diabetes, the number of islet autonomic nerves is upregulated. This review focuses on neural regulation of islet function, with emphasis on the neuropeptides.
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8.
  • Ahrén, Bo, et al. (författare)
  • Quantification of insulin secretion in relation to insulin sensitivity in nondiabetic postmenopausal women.
  • 2002
  • Ingår i: Diabetes. - : American Diabetes Association Inc.. - 1939-327X. ; 51:Suppl 1, s. 202-211
  • Tidskriftsartikel (refereegranskat)abstract
    • To evaluate mechanisms underlying the close association between insulin secretion and insulin sensitivity, insulin sensitivity was evaluated by the euglycemic-hyperinsulinemic clamp technique (M/I(clamp)) and insulin secretion was determined from the 75-g oral glucose tolerance test (OGTT) and from the glucose-dependent arginine-stimulation test in 81 nondiabetic postmenopausal women, all aged 61 years. M/I(clamp) was normally distributed with mean plus minus SD of 69.9 plus minus 30.5 nmol glucose center dot kg(-1) center dot min(-1)/pmol insulin center dot l(-1). It was found that the several different measures of insulin secretion from the OGTT and the glucose-dependent arginine-stimulation test were all inversely related to M/I(clamp). However, measures determining the direct insulin responses were more markedly potentiated by low M/I(clamp) than were measures determining glucose potentiation of insulin secretion. Moreover, the product of M/I(clamp) times measures of insulin secretion (disposition index [DI]) was inversely related to the 2-h glucose value. Finally, surrogate insulin sensitivity measures quantified from OGTT and the glucose-dependent arginine-stimulation test only weakly correlated to M/I(clamp) (R(2) approximate 0.25). Thus, 1) insulin secretion is adaptively increased when insulin sensitivity is low in nondiabetic postmenopausal women; 2) beta-cell exocytotic ability shows more efficient adaptation than beta-cell glucose recognition to low insulin sensitivity; 3) impaired beta-cell adaptation (i.e., low DI) is associated with higher 2-h glucose values during OGTT, although other regulatory mechanisms also exist; and 4) indirect surrogate measures of insulin sensitivity only weakly correlate to insulin sensitivity as determined by the euglycemic-hyperinsulinemic clamp.
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9.
  • Alanentalo, Tomas, et al. (författare)
  • Quantification and 3-D imaging of the insulitis-induced destruction of β-cells in murine type 1 diabetes
  • 2010
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 59:7, s. 1756-1764
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The aim of this study was to refine the information regarding the quantitative and spatial dynamics of infiltrating lymphocytes and remaining beta-cell volume during the progression of type 1 diabetes in the NOD mouse model of the disease.Research design and methods: Using an ex vivo technique, optical projection tomography (OPT), we quantified and assessed the 3D spatial development and progression of insulitis and beta-cell destruction in pancreas from diabetes prone NOD and non-diabetes prone congenic NOD.H-2b mice between 3 and 16 weeks of age.Results: Together with results showing the spatial dynamics of the insulitis process we provide data of beta-cell volume distributions down to the level of the individual islets and throughout the pancreas during the development and progression of type 1 diabetes. Our data provide evidence for a compensatory growth potential of the larger insulin(+) islets during the later stages of the disease around the time point for development of clinical diabetes. This is in contrast to smaller islets, which appear less resistant to the autoimmune attack. We also provide new information on the spatial dynamics of the insulitis process itself, including its apparently random distribution at onset, the local variations during its further development, and the formation of structures resembling tertiary lymphoid organs at later phases of insulitis progression.Conclusions: Our data provides a powerful tool for phenotypic analysis of genetic and environmental effects on type 1 diabetes etiology as well as for evaluating the potential effect of therapeutic regimes.
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10.
  • Alenkvist, Ida, et al. (författare)
  • Recruitment of Epac2A to Insulin Granule Docking Sites Regulates Priming for Exocytosis
  • 2017
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 66:10, s. 2610-2622
  • Tidskriftsartikel (refereegranskat)abstract
    • Epac is a cAMP-activated guanine nucleotide exchange factor that mediates cAMP signaling in various types of cells, including -cells, where it is involved in the control of insulin secretion. Upon activation, the protein redistributes to the plasma membrane, but the underlying molecular mechanisms and functional consequences are unclear. Using quantitative high-resolution microscopy, we found that cAMP elevation caused rapid binding of Epac2A to the -cell plasma membrane, where it accumulated specifically at secretory granules and rendered them more prone to undergo exocytosis. cAMP-dependent membrane binding required the high-affinity cyclic nucleotide-binding (CNB) and Ras association domains, but not the disheveled-Egl-10-pleckstrin domain. Although the N-terminal low-affinity CNB domain (CNB-A) was dispensable for the translocation to the membrane, it was critical for directing Epac2A to the granule sites. Epac1, which lacks the CNB-A domain, was recruited to the plasma membrane but did not accumulate at granules. We conclude that Epac2A controls secretory granule release by binding to the exocytosis machinery, an effect that is enhanced by prior cAMP-dependent accumulation of the protein at the plasma membrane.
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