scholarly journals Dietary glycemic load, glycemic index, and refined grains intake are associated with reduced β-cell function in prediabetic Japanese migrants

2009 ◽  
Vol 53 (4) ◽  
pp. 429-434 ◽  
Author(s):  
Daniela Saes Sartorelli ◽  
Laércio Joel Franco ◽  
Renata Damião ◽  
Suely Gimeno ◽  
Marly Augusto Cardoso ◽  
...  

OBJECTIVE: To investigate the association between carbohydrate intakes and β-cell function (HOMA-β) in Japanese-Brazilians with impaired glucose tolerance (IGT). METHODS: Dietary intakes were assessed by a validated food frequency questionnaire in a cross-sectional survey carried out in 2000. The associations between diet and HOMA-β were verified in 270 newly diagnosed IGT in multiple linear regression models. RESULTS: The mean (SD) age was 58 (11) years and the mean HOMA-β was 65 (47). The glycemic load was inversely associated with HOMA-β, β1 -0.140 (95%CI = -1.044; -0.078), p = 0.023. The inverse association was also observed for refined grains intakes: -0.186 (95%CI = -0.4862; -0.058), p = 0.012. After adjustments for body mass index, the glycemic index was inversely associated with HOMA-β: -0.1246 (95%CI = -2.2482, -0.0257), p < 0.001. CONCLUSIONS: These data suggested that dietary glycemic load, glycemic index, and refined grains intakes are associated with reduced β-cell function, and the quality of dietary carbohydrates may be relevant for maintaining β-cell function among individuals with IGT.

1980 ◽  
Vol 87 (2) ◽  
pp. 293-301 ◽  
Author(s):  
ABIGAIL L. FOWDEN ◽  
R. J. BARNES ◽  
R. S. COMLINE ◽  
MARIAN SILVER

Insulin secretion and the factors influencing β-cell function were investigated in the chronically catheterized fetal foal and mare during the second half of gestation. The response of the fetal β cells to exogenous glucose was also examined. The mean concentration of insulin in the fetal foal was 7·5 ± 0·5 (s.e.m.) μu./ml (n = 20) which was significantly less than the corresponding maternal value of 49·0 ± 5·0μu./ml (n = 20, P<0·01). The insulin concentration in non-pregnant horses was 24·5 ± 1·5 μu./ml (n = 5) which was significantly less than the value in the pregnant animals (P<0·01). However, there was no significant difference in the mean glucose concentration between the groups of adult animals. The insulin concentration was related to the endogenous glucose level in both adult and fetal horses. Wide variation in the maternal insulin concentration was observed above a glucose concentration of about 5·0 mmol/l. The mean concentration of insulin in pregnant mares decreased with increasing gestational age while the mean glucose concentration remained unaltered throughout the second half of gestation. There was no change in the basal concentrations of insulin or glucose in the fetus with gestational age although the fetal β-cell response to exogenous glucose appeared to increase with increasing fetal age after 270 days of gestation (term 330 days). There was a significant arterio-venous difference in the concentration of insulin across the gravid uterus in the mare when the arterial insulin level was greater than 30 μu./ml. Below this value, there was no consistent uptake of insulin by the uterus. The observations are discussed in relation to the regulation of insulin release in utero and the effects of pregnancy on maternal β-cell function.


2020 ◽  
Vol 34 (8) ◽  
pp. 107586
Author(s):  
Kristina M. Utzschneider ◽  
Tonya N. Johnson ◽  
Kara L. Breymeyer ◽  
Lisa Bettcher ◽  
Daniel Raftery ◽  
...  

2010 ◽  
Vol 163 (4) ◽  
pp. 551-558 ◽  
Author(s):  
Thomas G K Breuer ◽  
Bjoern A Menge ◽  
Matthias Banasch ◽  
Waldemar Uhl ◽  
Andrea Tannapfel ◽  
...  

IntroductionHyperproinsulinaemia has been reported in patients with type 2 diabetes. It is unclear whether this is due to an intrinsic defect in β-cell function or secondary to the increased demand on the β-cells. We investigated whether hyperproinsulinaemia is also present in patients with secondary diabetes, and whether proinsulin levels are associated with impaired β-cell area or function.Patients and methodsThirty-three patients with and without diabetes secondary to pancreatic diseases were studied prior to pancreatic surgery. Intact and total proinsulin levels were compared with the pancreatic β-cell area and measures of insulin secretion and action.ResultsFasting concentrations of total and intact proinsulin were similar in patients with normal, impaired (including two cases of impaired fasting glucose) and diabetic glucose tolerance (P=0.58 andP=0.98 respectively). There were no differences in the total proinsulin/insulin or intact proinsulin/insulin ratio between the groups (P=0.23 andP=0.71 respectively). There was a weak inverse association between the total proinsulin/insulin ratio and pancreatic β-cell area (r2=0.14,P=0.032), whereas the intact proinsulin/insulin ratio and the intact and total proinsulin levels were unrelated to β-cell area. However, a strong inverse relationship between homeostasis model assessment index of β-cell function and both the total and the intact proinsulin/insulin ratio was found (r2=0.55 andr2=0.48 respectively). The association of insulin resistance (IR) with intact proinsulin was much weaker than the correlation with fasting insulin.ConclusionsHyperproinsulinaemia is associated with defects in insulin secretion rather than a reduction in β-cell area. The weak association between intact proinsulin and IR argues against the usefulness of this parameter in clinical practice.


2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.


2004 ◽  
Vol 9 (4) ◽  
pp. 367-373
Author(s):  
Soo-Bong Choi ◽  
Chun-Hee Park ◽  
Dong-Wha Jun ◽  
Jin-Sun Jang ◽  
Sun-Min Park

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lina Sakhneny ◽  
Alona Epshtein ◽  
Limor Landsman

Abstractβ-Cells depend on the islet basement membrane (BM). While some islet BM components are produced by endothelial cells (ECs), the source of others remains unknown. Pancreatic pericytes directly support β-cells through mostly unidentified secreted factors. Thus, we hypothesized that pericytes regulate β-cells through the production of BM components. Here, we show that pericytes produce multiple components of the mouse pancreatic and islet interstitial and BM matrices. Several of the pericyte-produced ECM components were previously implicated in β-cell physiology, including collagen IV, laminins, proteoglycans, fibronectin, nidogen, and hyaluronan. Compared to ECs, pancreatic pericytes produce significantly higher levels of α2 and α4 laminin chains, which constitute the peri-islet and vascular BM. We further found that the pericytic laminin isoforms differentially regulate mouse β-cells. Whereas α2 laminins promoted islet cell clustering, they did not affect gene expression. In contrast, culturing on Laminin-421 induced the expression of β-cell genes, including Ins1, MafA, and Glut2, and significantly improved glucose-stimulated insulin secretion. Thus, alongside ECs, pericytes are a significant source of the islet BM, which is essential for proper β-cell function.


Sign in / Sign up

Export Citation Format

Share Document