scholarly journals Neighborhood walkability and risk of gestational diabetes

2020 ◽  
Vol 8 (1) ◽  
pp. e000938
Author(s):  
Simone Kew ◽  
Chang Ye ◽  
Sadia Mehmood ◽  
Anthony J Hanley ◽  
Mathew Sermer ◽  
...  
Keyword(s):  
Physical Activity ◽  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Maternal Risk ◽  
Neighborhood Walkability ◽  
Walk Score

ObjectiveHigher neighborhood walkability has been associated with a lower risk of type 2 diabetes mellitus (T2DM) by promoting greater physical activity (thereby reducing weight and lowering insulin resistance). However, it is not known if walkability may similarly reduce maternal risk of gestational diabetes mellitus (GDM), which arises in the setting of the severe physiologic insulin resistance of pregnancy. Indeed, the insulin resistance of pregnancy is primarily driven by placental hormones and not maternal weight gain. Thus, we sought to evaluate the impact of neighborhood walkability on maternal risk of GDM and the pathophysiologic determinants thereof (insulin sensitivity and pancreatic beta-cell function).MethodsIn this study, 1318 women reported their pregravid physical activity (Baecke questionnaire) while undergoing an oral glucose tolerance test (OGTT) at mean 29.3 weeks’ gestation. The OGTT identified 290 women with GDM and enabled assessment of insulin sensitivity and beta-cell function. Based on their residential Walk Score, the women were stratified into the following four established categories of neighborhood walkability: car dependent (n=328), somewhat walkable (n=315), very walkable (n=406), and walker’s paradise (n=269).ResultsThere was a progressive increase in pregravid total physical activity (p=0.002), non-sport leisure-time activity (p=0.009) and sport activity (p=0.01) across the walkability groups (from car dependent to somewhat walkable to very walkable to walker’s paradise), coupled with a concomitant decline in pre-pregnancy body mass index (p=0.007). However, in pregnancy, the groups did not differ in gestational weight gain (p=0.80). Moreover, the walkability groups also did not differ in mean adjusted insulin sensitivity, beta-cell function, or glycemia on the antepartum OGTT. On logistic regression analysis, Walk Score did not predict GDM (OR=1.001, 95% CI 0.995 to 1.007).ConclusionNeighborhood walkability is not a significant determinant of maternal risk of GDM. Thus, in contrast to T2DM, the effect of neighborhood design on incidence of GDM will be comparatively modest.

scholarly journals Longitudinal changes in insulin sensitivity and beta cell function between women with and without a history of gestational diabetes mellitus

Diabetologia ◽  
2013 ◽  
Vol 56 (12) ◽  
pp. 2753-2760 ◽  
Author(s):  
Anny H. Xiang ◽  
Miwa Takayanagi ◽  
Mary Helen Black ◽  
Enrique Trigo ◽  
Jean M. Lawrence ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Sensitivity ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Longitudinal Changes ◽  
History Of

scholarly journals Biomarkers of subclinical inflammation and increases in glycaemia, insulin resistance and beta-cell function in non-diabetic individuals: the Whitehall II study

2016 ◽  
Vol 175 (5) ◽  
pp. 367-377 ◽  
Author(s):  
Christian Herder ◽  
Kristine Færch ◽  
Maren Carstensen-Kirberg ◽  
Gordon D Lowe ◽  
Rita Haapakoski ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fasting Insulin ◽  
Subclinical Inflammation ◽  
Increased Risk

Objective Higher systemic levels of pro-inflammatory biomarkers and low adiponectin are associated with increased risk of type 2 diabetes, but their associations with changes in glycaemic deterioration before onset of diabetes are poorly understood. We aimed to study whether inflammation-related biomarkers are associated with 5-year changes in glucose and insulin, HbA1c, insulin sensitivity and beta-cell function before the diagnosis of type 2 diabetes and whether these associations may be bidirectional. Design and methods We used multiple repeat measures (17 891 person-examinations from 7683 non-diabetic participants) from the Whitehall II study to assess whether circulating high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), IL1 receptor antagonist (IL1Ra) and adiponectin are associated with subsequent changes in glycaemia, insulin, insulin resistance and beta-cell function (based on oral glucose tolerance tests). We examined bidirectionality by testing if parameters of glucose metabolism at baseline are associated with changes in inflammation-related biomarkers. Results Higher hsCRP and IL6 were associated with increases in fasting insulin, insulin resistance and, for IL6, with beta-cell function after adjustment for confounders. Higher adiponectin was associated with decreases in fasting glucose, HbA1c, fasting insulin, insulin resistance and beta-cell function. The reverse approach showed that 2-h glucose and insulin sensitivity were associated with changes in IL1Ra. Fasting insulin and insulin resistance showed inverse associations with changes in adiponectin. Conclusions Subclinical inflammation is associated with development of increased glycaemia, insulin resistance and beta-cell function in non-diabetic individuals. These findings are consistent with the hypothesis that inflammation-related processes may increase insulin resistance and lead to a compensatory upregulation of beta-cell function.

scholarly journals Diabetic macro- and microvascular disease in type 2 diabetes

2007 ◽  
Vol 4 (2_suppl) ◽  
pp. S7-S11 ◽  
Author(s):  
Michel P Hermans
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Microvascular Disease ◽  
Patients With Diabetes

Before a patient develops overt type 2 diabetes mellitus, there is typically a prolonged period of patho-physiological change. In the common form of type 2 diabetes mellitus, there are years of insulin resistance, initially compensated by increased beta cell function, then impaired glucose tolerance develops, and finally type 2 diabetes. We know from studies such as the United Kingdom Prospective Diabetes Study (UKPDS) and the Belfast study that loss of beta cell function and insulin resistance are usually relentless.1, 2 Thus, therapy to reduce blood glucose has to be gradually increased with time for patients with diabetes. What is less well known is that every person has a different slope for beta cell function loss which intersects with insulin resistance.

scholarly journals Clinical phenotyping of newly diagnosed type 2 diabetes in Yemen

2018 ◽  
Vol 6 (1) ◽  
pp. e000587 ◽  
Author(s):  
Abdallah Ahmed Gunaid ◽  
Mohammed Mohammed Al-Kebsi ◽  
Mahfouth Abdalla Bamashmus ◽  
Saleh Ahmed Al-Akily ◽  
Ahmed Nasser Al-Radaei
Keyword(s):  
Insulin Resistance ◽  
Cluster Analysis ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Clinical Variables ◽  
High Insulin ◽  
Function Group ◽  
Cluster 2

ObjectiveTo identify clinical phenotypes of type 2 diabetes (T2D) among adults presenting with a first diagnosis of diabetes.Research design and methodsA total of 500 consecutive patients were subject to clinical assessment and laboratory investigations. We used data-driven cluster analysis to identify phenotypes of T2D based on clinical variables and Homeostasis Model Assessment (HOMA2) of insulin sensitivity and beta-cell function estimated from paired fasting blood glucose and specific insulin levels.ResultsThe cluster analysis identified three statistically different clusters: cluster 1 (high insulin resistance and high beta-cell function group), which included patients with low insulin sensitivity and high beta-cell function; cluster 2 (low insulin resistance and low beta-cell function group), which included patients with high insulin sensitivity but very low beta-cell function; and cluster 3 (high insulin resistance and low beta-cell function group), which included patients with low insulin sensitivity and low beta-cell function. Insulin sensitivity, defined as median HOMA2-S, was progressively increasing from cluster 1 (35.4) to cluster 3 (40.9), to cluster 2 (76) (p<0.001). On the contrary, beta-cell function, defined as median HOMA2-β, was progressively declining from cluster 1 (78.3) to cluster 3 (30), to cluster 2 (22.3) (p<0.001). Clinical and biomarker variables associated with insulin resistance like obesity, abdominal adiposity, fatty liver, and high serum triglycerides were mainly seen in clusters 1 and 3. The highest median hemoglobin A1c value was noted in cluster 2 (88 mmol/mol) and the lowest in cluster 1.ConclusionCluster analysis of newly diagnosed T2D in adults has identified three phenotypes based on clinical variables central to the development of diabetes and on specific clinical variables of each phenotype.

scholarly journals Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Abdel-Baset M. Aref ◽  
Osama M. Ahmed ◽  
Lobna A. Ali ◽  
Margit Semmler
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Maternal Diabetes ◽  
Serum Glucose ◽  
Time Intervals ◽  
Rat Offspring ◽  
Normal Rat

This study was designed to assess the effect of maternal diabetes in rats on serum glucose and insulin concentrations, insulin resistance, histological architecture of pancreas and glycogen content in liver of offspring. The pregnant rat females were allocated into two main groups: normal control group and streptozotocin-induced diabetic group. After birth, the surviving offspring were subjected to biochemical and histological examination immediately after delivery and at the end of the 1st and 2nd postnatal weeks. In comparison with the offspring of normal control dams, the fasting serum glucose level of offspring of diabetic mothers was significantly increased at the end of the 1st and 2nd postnatal weeks. Serum insulin level of offspring of diabetic dams was significantly higher at birth and decreased significantly during the following 2 postnatal weeks, while in normal rat offspring, it was significantly increased with progress of time. HOMA Insulin Resistance (HOMA-IR) was significantly increased in the offspring of diabetic dams at birth and after 1 week than in normal rat offspring, while HOMA insulin sensitivity (HOMA-IS) was significantly decreased. HOMA beta-cell function was significantly decreased at all-time intervals in offspring of diabetic dams. At birth, islets of Langerhans as well as beta cells in offspring of diabetic dams were hypertrophied. The cells constituting islets seemed to have a high division rate. However, beta-cells were degenerated during the following 2 post-natal weeks and smaller insulin secreting cells predominated. Vacuolation and necrosis of the islets of Langerhans were also observed throughout the experimental period. The carbohydrate content in liver of offspring of diabetic dams was at all-time intervals lower than that in control. The granule distribution was more random. Overall, the preexisting maternal diabetes leads to glucose intolerance, insulin resistance, and impaired insulin sensitivity andβ-cell function in the offspring at different postnatal periods.

Sign in / Sign up

Export Citation Format

Share Document