scholarly journals Incretin Effect in Women with Former Gestational Diabetes within a Short Period after Delivery

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
G. Pacini ◽  
A. Tura ◽  
Y. Winhofer ◽  
A. Kautzky-Willer
Keyword(s):  
Gestational Diabetes ◽  
Beta Cell ◽  
Cell Function ◽  
Normal Pregnancy ◽  
Incretin Effect ◽  
Cell Dysfunction ◽  
Short Period ◽  
Glucose Test

Background and Aims. Women with former gestational diabetes (fGDM) are characterized by impaired beta-cell function (BC). Incretin hormones contribute to insulin secretion after oral administration of glucose. We aimed to assess the possible role of incretins on altered insulin release in fGDM.Materials and Methods. We studied 104 fGDM women within 6 months after delivery and 35 healthy women after normal pregnancy (CNT) with a 75 g oral (OGTT) and a 0.33 g/kg intravenous (IVGTT) glucose test, both lasting 3 h. The ratio of suprabasal areas under the concentration curves for glucose (dAUCGL) and C-peptide (dAUCCP) evaluated BC during OGTT (BCOG) and IVGTT (BCIV). Incretin effect was computed in all fGDM and in fGDM with normal tolerance (fGDMNGT) and with impaired glucose regulation (fGDMIGR).Results.dAUCGLof fGDM was higher (P<0.0001) than CNT for both tests; whiledAUCCPwere not different.BCOGandBCIVwere lower in fGDM versus CNT (1.42±0.17nmolCP/mmolGLUCversus2.53±0.61,P=0.015and0.41±0.03versus0.68±0.10,P=0.0006, respectively). IE in CNT (66±4 %) was not different from that of all fGDM (59±3) andfGDMNGT(60±3), but higher than that offGDMIGR(52±6;P=0.03). IE normalized to BMI was2.77±0.19 % m2/kg in CNT, higher than that offGDMIGR(1.75±0.21;P=0.02) and also offGDMNGT  (2.33±0.11;P=0.038).Conclusion. Compromised IE characterizesfGDMIGR. In both fGDM categories, regardless their glucose tolerance, IE normalized to BMI was reduced, signifying an intrinsic characteristic of fGDM. Therefore, the diminished IE of fGDM seems to reflect an early abnormality of the general beta-cell dysfunction in the progression toward type 2 diabetes.

scholarly journals The central role of calcium in the effects of cytokines on beta-cell function: Implications for type 1 and type 2 diabetes

Cell Calcium ◽  
2011 ◽  
Vol 50 (6) ◽  
pp. 481-490 ◽  
Author(s):  
James W. Ramadan ◽  
Stephen R. Steiner ◽  
Christina M. O’Neill ◽  
Craig S. Nunemaker
Keyword(s):  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function

scholarly journals Recovery of the Incretin Effect in Type 2 Diabetic Patients After Biliopancreatic Diversion

2015 ◽  
Vol 100 (5) ◽  
pp. 1984-1988 ◽  
Author(s):  
Fernanda S. Novaes ◽  
Ana C. J. Vasques ◽  
José C. Pareja ◽  
Filip K. Knop ◽  
Andrea Tura ◽  
...  
Keyword(s):  
Beta Cell ◽  
Biliopancreatic Diversion ◽  
Beta Cell Function ◽  
Cell Function ◽  
Diabetic Patients ◽  
Obese Patients ◽  
Incretin Effect ◽  
Intravenous Glucose ◽  
The Impact

Abstract Context: Bariatric surgery often results in remission of the diabetic state in obese patients. Increased incretin effect seems to play an important role in the glycemic improvements after Roux-en-Y gastric bypass, but the impact of biliopancreatic diversion (BPD) remains unexplored. Objective: The objective was to elucidate the effect of BPD on the incretin effect and its interplay with beta-cell function and insulin sensitivity (IS) in obese subjects with type 2 diabetes (T2DM). Design, Setting and Patients: Twenty-three women were studied: a control group of 13 lean, normal glucose-tolerant women (lean NGT) studied once and 10 obese patients with T2DM studied before, 1 and 12 months after BPD. Intervention: The ObeseT2DM group underwent BPD. Main Outcome Measures: The main outcome measure was the change in incretin effect as measured by the isoglycemic intravenous glucose infusion test. Secondary outcomes encompassed IS and beta-cell function. Results: At baseline, the incretin effect was lower in obese T2DM compared to lean NGT (P &lt; .05). One month after BPD, the incretin effect was not changed, but at 12 months it reached the level of the lean NGT group (P &gt; .05). IS improved (P &lt; .05) 1 month after BPD and at 12 months it resembled the levels of the lean NGT group. Insulin secretory rate and beta-cell glucose sensitivity increased after BPD and achieved levels similar to lean NGT group 1 month after BPD and even higher levels at 12 months (P &lt; .05). Conclusions: BPD has no acute impact on the reduced incretin effect, but 12 months after surgery the incretin effect normalizes alongside normalization of glucose control, IS and beta-cell function.

scholarly journals JOE DOUPE LECTURE: Emerging Strategies for the Preservation of Pancreatic Beta-cell Function in early Type 2 Diabetes

2014 ◽  
Vol 37 (6) ◽  
pp. 414 ◽  
Author(s):  
Ravi Retnakaran
Keyword(s):  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fundamental Problem ◽  
Pancreatic Beta Cell ◽  
Beta Cell Dysfunction ◽  
Cell Dysfunction ◽  
Pancreatic Beta Cell Function

A fundamental problem in the clinical management of type 2 diabetes is the inability to prevent the ongoing deterioration of pancreatic beta-cell function over time that underlies the chronic progressive nature of this condition. Importantly, beta-cell dysfunction has both reversible and irreversible components. Furthermore, the amelioration of reversible beta-cell dysfunction through the early institution of short-term insulin-based therapy has emerged as a strategy that can yield temporary remission of type 2 diabetes. In this context, we have forwarded a novel therapeutic paradigm consisting of initial induction therapy to improve beta-cell function early in the course of diabetes followed by maintenance therapy aimed at preserving this beneficial beta-cell effect. Ultimately, this approach may yield an optimized therapeutic strategy for the durable preservation of beta-cell function and consequent modification of the natural history of type 2 diabetes.

scholarly journals No detectable effect of a type 2 diabetes-associated TCF7L2 genotype on the incretin effect

2020 ◽  
Vol 9 (12) ◽  
pp. 1221-1232
Author(s):  
David S Mathiesen ◽  
Jonatan I Bagger ◽  
Katrine B Hansen ◽  
Anders E Junker ◽  
Astrid Plamboeck ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Beta Cell ◽  
Cell Function ◽  
Tolerance Test ◽  
Detectable Effect ◽  
Oral Glucose ◽  
Incretin Effect ◽  
Intravenous Glucose ◽  
Elevated Glucose

The T allele of TCF7L2 rs7903146 is a common genetic variant associated with type 2 diabetes (T2D), possibly by modulation of incretin action. In this study, we evaluated the effect of the TCF7L2 rs7903146 T allele on the incretin effect and other glucometabolic parameters in normal glucose tolerant individuals (NGT) and participants with T2D. The rs7903146 variant was genotyped in cohorts of 61 NGT individuals (23 were heterozygous (CT) or homozygous (TT) T allele carriers) and 43 participants with T2D (20 with CT/TT). Participants were previously examined by an oral glucose tolerance test (OGTT) and a subsequent isoglycemic intravenous glucose infusion (IIGI). The incretin effect was assessed by quantification of the difference in integrated beta cell secretory responses during the OGTT and IIGI. Glucose and hormonal levels were measured during experimental days, and from these, indices of beta cell function and insulin sensitivity were calculated. No genotype-specific differences in the incretin effect were observed in the NGT group (P = 0.70) or the T2D group (P = 0.68). NGT T allele carriers displayed diminished glucose-dependent insulinotropic polypeptide response during OGTT (P = 0.01) while T allele carriers with T2D were characterized by lower C-peptide AUC after OGTT (P = 0.04) and elevated glucose AUC after OGTT (P = 0.04). In conclusion, our findings do not exclude that this specific TCF7L2 variant increases the risk of developing T2D via diminished incretin effect, but genotype-related defects were not detectable in these cohorts.

scholarly journals The Role of Vegan Diets in Lipotoxicity-Induced Beta-Cell Dysfunction in Type-2-Diabetes

2020 ◽  
Vol 27 (SP2) ◽  
pp. e22-e38
Author(s):  
Maximilian Andreas Storz
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Beta Cell ◽  
Beta Cells ◽  
Beta Cell Function ◽  
Cell Function ◽  
Beta Cell Dysfunction ◽  
Cell Dysfunction

Type-2-diabetes is considered the new plague of the current century and both, its incidence and prevalence are rapidly increasing. Chronic insulin resistance and a progressive decline in beta-cell function are discussed as the root causes of type-2-diabetes. Both were associated with obesity and pathologically elevated concentrations of circulating free fatty acids in the blood. The harmful effects of chronically elevated free fatty acid levels on glucose homeostasis and non-adipose tissues are referred to as lipotoxicity. Pancreatic beta-cells appear to be particularly vulnerable and both, dietary fat quantity and quality may impact beta-cell function. Diets high in saturated fats are especially harmful to beta-cells while (poly-)unsaturated fatty acids were associated with beta-cell protective effects. This review examined how a dietary modification towards a low-fat vegan diet, which is particularly low in saturated and trans-fats, could help to prevent or reduce lipotoxicity-induced beta cell dysfunction. Several potential mechanisms of action were identified including: (1) reduced total fat intake (fat quantity), (2) a more favorable polyunsaturated fatty acid to saturated fatty acid ratio (fat quality), (3) improved body weight and a reduction in adipose tissue mass, and finally (4) improved glycemic control. The latter appears of paramount importance in light of the accumulating evidence that lipotoxic events are tightly coupled to excess glucose levels. All four mechanisms are likely to contribute complementarily to improved beta-cell function in individuals with type-2-diabetes and may reduce the likelihood of lipotoxic events to occur. Physicians must consider these findings when counseling patients on lifestyle and nutrition.

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