scholarly journals Dramatic recovery without steroid therapy and withdrawal from insulin therapy in a subject with hyperglycemic and hyperosmolar syndrome and depletion of insulin secretory capacity induced by type 2 autoimmune pancreatitis

Medicine ◽  
2022 ◽  
Vol 101 (2) ◽  
pp. e28609
Author(s):  
Yuichiro Iwamoto ◽  
Fuminori Tatsumi ◽  
Kenji Kohara ◽  
Masashi Shimoda ◽  
Shuhei Nakanishi ◽  
...  
Keyword(s):  
Insulin Therapy ◽  
Steroid Therapy ◽  
Autoimmune Pancreatitis ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

scholarly journals Association between Pancreatic Atrophy and Loss of Insulin Secretory Capacity in Patients with Type 2 Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Jun Lu ◽  
Meixiang Guo ◽  
Hongtao Wang ◽  
Haibin Pan ◽  
Liang Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Multiple Logistic Regression Analysis ◽  
Insulin Deficiency ◽  
Cross Sectional ◽  
Pancreatic Atrophy ◽  
Insulin Secretory Capacity ◽  
Absolute Insulin Deficiency ◽  
Secretory Capacity

Aims. To examine pancreatic volume (PV) changes among patients with different duration of type 2 diabetes and whether pancreatic atrophy was associated with loss of insulin secretory capacity. Methods. This cross-sectional study (203 patients with type 2 diabetes, 93 controls without diabetes) was conducted from January 2016 to December 2017. Patients with type 2 diabetes were divided into 3 groups: recently diagnosed (duration≤2 years), midterm (duration 3-9 years), and long term (duration≥10 years). All the patients were scanned with upper abdominal computerized tomography; PV was then calculated by an experienced technician. Absolute insulin deficiency was defined as fasting C−peptide<0.9 ng/mL. Results. Compared with PV (cm3) in the controls, the mean PV was similar in patients with recently diagnosed type 2 diabetes (68.8 versus 71.0, P=0.56) but significantly reduced in patients with midterm (68.8 versus 60.8, P<0.05) and long-term (68.8 versus 53.1, P<0.001) type 2 diabetes. A similar trend was observed for the PV index (PV adjusted for body surface area and body mass index). Furthermore, rates of pancreatic atrophy and absolute insulin deficiency increased with duration of diabetes. Multiple logistic regression analysis indicated that pancreatic atrophy was associated with higher likelihood of absolute insulin deficiency (odds ratio=4.47, 95%confidence interval=1.45‐13.8). Conclusions. PV was reduced in those with midterm and long-term type 2 diabetes compared to individuals without type 2 diabetes. Overall, pancreatic atrophy was associated with the loss of insulin secretory capacity in patients with type 2 diabetes.

scholarly journals Leptin and Other Factors as Determinants of Insulin Secretion and Sensitivity in Bangladeshi Type 2 Diabetic Subjects

1970 ◽  
Vol 3 ◽  
pp. 1-7
Author(s):  
Manindra Nath Roy ◽  
Salima Akter ◽  
Mohammad Jafarulla ◽  
Forhadul Hoque Mollah ◽  
Ajanta Rani Saha ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
B Cell ◽  
Plasma Glucose ◽  
Key Words Leptin ◽  
Type 2 Diabetic ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

Background: The relative contribution of insulin secretion and sensitivity in the development of Type 2 diabetes mellitus (T2DM) vary from population to population due to the heterogeneous nature of the disease. The study was undertaken to evaluate insulin secretory capacity and sensitivity in a Bangladeshi Type 2 diabetic population and to explore the association of some of the anthropometric and biochemical factors known to modulate B-cell function and insulin action. Methods: Ninety one T2DM subjects and 32 age-matched controls were studied for their fasting plasma glucose (FPG), lipids, HbA1c (by HPLC), leptin and C-peptide (ELISA). Insulin secretion (HOMA B) and insulin sensitivity (HOMA S) were calculated by homeostasis model assessment (HOMA). Results: Both insulin secretion and sensitivity were significantly reduced in diabetic as compared to control (HOMA B%, geometric mean±SD, 35.65±1.75 vs. 96.29±1.50, p < 0.001; HOMA S%, 68.66±1.71 vs. 104.951.63, p < 0.001). However, B-cell dysfunction was predominant than insulin resistance in predicting T2DM as the discriminate function coefficient for HOMA B (1.098) was greater than that for HOMA S (0.821). In T2DM, HOMA B had positive correlation with BMI (r=0.368, p < 0.001) and HOMA S was inversely correlated to BMI (r=-0.261, p < 0.01), WHR (r=-0.258, p < 0.01) and plasma TG (r=-0.233, p < 0.001). On multiple regression analysis HOMA B and HOMA S were found to be inversely associated to FPG (p < 0.001) and leptin (p < 0.05) in T2DM. Conclusions: Both insulin secretory dysfunction and insulin resistance are present in Bangladeshi T2DM subjects, but B-cell failure seems to be the predominant abnormality. BMI, plasma glucose, insulin and leptin are the major determinants of insulin secretory capacity and generalized as well as central obesity, plasma glucose, triglycerides, insulin and leptin are among the major determinants of insulin sensitivity in this population. Key Words: Leptin, Insulin, Diabetes   doi: 10.3329/jbsp.v3i0.1786 J Bangladesh Soc Physiol. 2008 Dec;(3):1-7.

Classification of Type 1 and Type 2 Diabetes Mellitus from Studies of ICA, HLA and Insulin Secretory Capacity

1987 ◽  
Vol 29 (3) ◽  
pp. 340-344
Author(s):  
Nobuo Matsuura ◽  
Kenji Fujieda ◽  
Yuhei Mikami ◽  
Hiroko Fujita ◽  
Shohei Harada ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

scholarly journals Preserved Insulin Secretory Capacity and Weight Loss Are the Predominant Predictors of Glycemic Control in Patients With Type 2 Diabetes Randomized to Roux-en-Y Gastric Bypass

Diabetes ◽  
2015 ◽  
Vol 64 (9) ◽  
pp. 3104-3110 ◽  
Author(s):  
Kim T. Nguyen ◽  
Charles J. Billington ◽  
Adrian Vella ◽  
Qi Wang ◽  
Leaque Ahmed ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Loss ◽  
Gastric Bypass ◽  
Glycemic Control ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

scholarly journals Pancreatic β-Cell Rest Replenishes Insulin Secretory Capacity and Attenuates Diabetes in an Extreme Model of Obese Type 2 Diabetes

Diabetes ◽  
2018 ◽  
Vol 68 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Brandon B. Boland ◽  
Charles Brown ◽  
Michelle L. Boland ◽  
Jennifer Cann ◽  
Michal Sulikowski ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Extreme Model ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

scholarly journals Morphology of the pancreas in type 2 diabetes: effect of weight loss with or without normalisation of insulin secretory capacity

Diabetologia ◽  
2016 ◽  
Vol 59 (8) ◽  
pp. 1753-1759 ◽  
Author(s):  
Ahmad Al-Mrabeh ◽  
Kieren G. Hollingsworth ◽  
Sarah Steven ◽  
Roy Taylor
Keyword(s):  
Type 2 Diabetes ◽  
Weight Loss ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

scholarly journals Interorgan Crosstalk Contributing to β-Cell Dysfunction

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Katsuya Tanabe ◽  
Kikuko Amo-Shiinoki ◽  
Masayuki Hatanaka ◽  
Yukio Tanizawa
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Current Knowledge ◽  
Cell Mass ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Circulating Levels ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

Type 2 diabetes mellitus (T2DM) results from pancreatic β-cell failure in the setting of insulin resistance. In the early stages of this disease, pancreatic β-cells meet increased insulin demand by both enhancing insulin-secretory capacity and increasing β-cell mass. As the disease progresses, β-cells fail to maintain these compensatory responses. This involves both extrinsic signals and mediators intrinsic to β-cells, which adversely affect β-cells by impairing insulin secretion, decreasing proliferative capacities, and ultimately causing apoptosis. In recent years, it has increasingly been recognized that changes in circulating levels of various factors from other organs play roles in β-cell dysfunction and cellular loss. In this review, we discuss current knowledge of interorgan communications underlying β-cell failure during the progression of T2DM.

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