scholarly journals SERUM VISFATIN, INSULIN RESISTANCE AND BETA CELL FUNCTION IN TYPE II DIABETIC PATIENTS AND NON-DIABETIC ADULT OFFSPRING WITH POSITIVE PARENTAL HISTORY OF TYPE II DIABETES MELLITUS

2021 ◽  
Vol 32 (01) ◽  
pp. 22-27
Author(s):  
Tashfeen Ikram ◽  
Muniza Saeed ◽  
Sabiha Iqbal ◽  
Zunairah Hamayun ◽  
Hifza Noor Lodhi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Diabetic Patients ◽  
Adult Offspring ◽  
Type Ii ◽  
Group Iii ◽  
Group I ◽  
Type Ii Diabetics

Introduction: Non-diabetic individuals with type II diabetic parents are more susceptible to develop Diabetes. Visfatin; an adipocytokine and an enzyme is linked with glucose metabolism and affected by obesity. It works like insulin in the human body.  It serves as a key enzyme in nicotinamide adenine dinucleotide biosynthesis and plays a pivotal role in glucose mediated insulin secretion. Aims and Objectives: In this study we aimed to determine and compare serum visfatin levels, insulin resistance (HOMA-IR) and beta cell function (HOMA-%B) of type II diabetic patients and non-diabetic adult offspring of type II diabetic parents with that of non-diabetic adult offspring of non-diabetic parents. Material and methods It was a cross-sectional comparative study conducted at Diabetes clinic of Lahore General Hospital (LGH) and department of Physiology, Post Graduate Medical Institute (PGMI), Lahore in 2018. The study groups included thirty type II diabetic subjects (group III) and forty non-diabetic adult offspring of type II diabetic parents (group II). Forty non-diabetic adult offspring of non-diabetic parents served as controls (group I). The subjects were of thirty to fifty years of age. Blood pressure, BMI and waist circumference of every subject was measured. Fasting blood samples of the subjects were analyzed for serum insulin, glucose and visfatin. Insulin resistance (HOMA-IR), insulin sensitivity (HOMA-%S) and beta cell function (HOMA-%β) were also calculated. Results Type II diabetics (group III) had significantly higher serum visfatin, HOMA-IR, and lower HOMA-%S as compared to the controls (group I). No significant difference was found between HOMA-%B of group III and controls. On the contrary, non-diabetic adult offspring of type II diabetic parents (group II) had significantly lower serum visfatin and HOMA-%S while HOMA-%β, HOMA-IR was significantly higher in comparison to the control group (group I). Conclusion Visfatin production seems suppressed in non-diabetic individuals with type II diabetic parents probably due to hyperinsulinemia. Moreover, it has a little role in insulin secretion in these individuals as reflected by their higher HOMA-%B index. However, visfatin’s upregulation in chronic hyperglycemia is indicative of its restorative role in the declined beta-cell function in type II diabetics.

scholarly journals Serum CA19-9 Level Associated with Metabolic Control and Pancreatic Beta Cell Function in Diabetic Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Haoyong Yu ◽  
Ruixia Li ◽  
Lei Zhang ◽  
Haibing Chen ◽  
Yuqian Bao ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Beta Cell ◽  
Total Cholesterol ◽  
Beta Cell Function ◽  
Cell Function ◽  
Total Cholesterol Level ◽  
Pancreatic Beta Cell ◽  
Elevated Serum ◽  
Diabetic Patients ◽  
Pancreatic Beta Cell Function

CA19-9 is a tumor-associated antigen. It is also a marker of pancreatic tissue damage that might be caused by diabetes. Long-term poor glycemic control may lead to pancreatic beta cell dysfunction which is reflected by elevated serum CA19-9 level. Intracellular cholesterol accumulation leads to islet dysfunction and impaired insulin secretion which provide a new lipotoxic model. This study firstly found total cholesterol was one of the independent contributors to CA19-9. Elevated serum CA19-9 level in diabetic patients may indicate further investigations of glycemic control, pancreatic beta cell function, and total cholesterol level.

Insulin resistance and beta cell function in aboriginals with type 2 diabetes in Atlantic Canada

2000 ◽  
Vol 50 ◽  
pp. 108 ◽  
Author(s):  
Meng H. Tan ◽  
Sethu Reddy ◽  
Jean Abram ◽  
Pantelis Andreou ◽  
Danita Volder
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Atlantic Canada

scholarly journals Sustained Improvements in Glucose Metabolism Late After Roux-En-Y Gastric Bypass Surgery in Patients with and Without Preoperative Diabetes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nils B. Jørgensen ◽  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Christoffer Martinussen ◽  
Maria S. Svane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Relative Change

Abstract To describe glucose metabolism in the late, weight stable phase after Roux-en-Y Gastric Bypass (RYGB) in patients with and without preoperative type 2 diabetes we invited 55 RYGB-operated persons from two existing cohorts to participate in a late follow-up study. 44 (24 with normal glucose tolerance (NGT)/20 with type 2 diabetes (T2D) before surgery) accepted the invitation (median follow-up 2.7 [Range 2.2–5.0 years]). Subjects were examined during an oral glucose stimulus and results compared to preoperative and 1-year (1 y) post RYGB results. Glucose tolerance, insulin resistance, beta-cell function and incretin hormone secretion were evaluated. 1 y weight loss was maintained late after surgery. Glycemic control, insulin resistance, beta-cell function and GLP-1 remained improved late after surgery in both groups. In NGT subjects, nadir glucose decreased 1 y after RYGB, but did not change further. In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. In NGT subjects, relative changes in postprandial nadir glucose correlated with changes in beta-cell glucose sensitivity. Thus, effects of RYGB on weight and glucose metabolism are maintained late after surgery in patients with and without preoperative T2D. Weight loss and improved beta-cell function both contribute to maintenance of long-term glycemic control in patients with type 2 diabetes, and increased glucose stimulated insulin secretion may contribute to postprandial hypoglycemia in NGT subjects.

Beta-cell function and insulin resistance evaluated by HOMA in pancreatic cancer subjects with varying degrees of glucose intolerance

Pancreatology ◽  
2005 ◽  
Vol 5 (2-3) ◽  
pp. 229-233 ◽  
Author(s):  
Suresh T. Chari ◽  
Mauricio Zapiach ◽  
Dhiraj Yadav ◽  
Robert A. Rizza
Keyword(s):  
Insulin Resistance ◽  
Pancreatic Cancer ◽  
Beta Cell ◽  
Glucose Intolerance ◽  
Beta Cell Function ◽  
Cell Function
Sign in / Sign up

Export Citation Format

Share Document