scholarly journals New Therapeutic Approaches to Prevent or Delay Beta-Cell Failure in Diabetes

2015 ◽  
Vol 22 (3) ◽  
pp. 311-319
Author(s):  
Floriana Elvira Ionica
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
International Diabetes Federation ◽  
The Body ◽  
Therapeutic Approaches ◽  
Therapeutic Modalities ◽  
Beta Cell Failure ◽  
New Therapeutic Approaches

AbstractBackground and aims: The most recent estimates of International Diabetes Federation indicate that 382 million people have diabetes, and the incidence of this disease is increasing. While in type 1 diabetes mellitus (T1DM) beta-cell death is autoimmunemediated, type 2 diabetes mellitus (T2DM) results from an interaction between genetic and environmental factors that impair beta-cell function and insulin action. Many people with T2DM remain unaware of their illness for a long time because symptoms may take years to appear or be recognized, while the body is affected by excess blood glucose. These patients are often diagnosed only when diabetes complications have already developed. The aim of this article was to perform a review based on literature data on therapeutic modalities to prevent/delay beta cell function decline. Material and Methods: We searched MEDLINE from 2000 to the present to identify the therapeutic approaches to prevent or delay beta-cell failure in patients with T2DM. Results and conclusions: Several common polymorphisms in genes linked to monogenic forms of diabetes appear to influence the response to T2DM pharmacotherapy. Recent studies report the role of the G protein coupled receptor 40 (GPR40), also known as Free Fatty Acids Receptor 1 (FFAR1) in the regulation of beta-cell function- CNX-011-67 (a GPR40 agonist) has the potential to provide good and durable glycemic control in T2DM patients.

Pantoprazole may improve beta cell function and diabetes mellitus

2014 ◽  
Vol 37 (5) ◽  
pp. 449-454 ◽  
Author(s):  
F. Inci ◽  
M. Atmaca ◽  
M. Ozturk ◽  
S. Yildiz ◽  
R. Koceroglu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function

scholarly journals A Triple Threat? The Role of Diet, Nutrition, and the Microbiota in T1D Pathogenesis

2021 ◽  
Vol 8 ◽  
Author(s):  
Emma E. Hamilton-Williams ◽  
Graciela L. Lorca ◽  
Jill M. Norris ◽  
Jessica L. Dunne
Keyword(s):  
Beta Cell ◽  
Intestinal Microbiota ◽  
Beta Cell Function ◽  
Cell Function ◽  
The Body ◽  
Islet Autoimmunity ◽  
Potential Mechanism ◽  
Modifiable Factors ◽  
And Function

In recent years the role of the intestinal microbiota in health and disease has come to the forefront of medical research. Alterations in the intestinal microbiota and several of its features have been linked to numerous diseases, including type 1 diabetes (T1D). To date, studies in animal models of T1D, as well as studies in human subjects, have linked several intestinal microbiota alterations with T1D pathogenesis. Features that are most often linked with T1D pathogenesis include decreased microbial diversity, the relative abundance of specific strains of individual microbes, and altered metabolite production. Alterations in these features as well as others have provided insight into T1D pathogenesis and shed light on the potential mechanism by which the microbiota plays a role in T1D pathogenesis, yet the underlying factors leading to these alterations remains unknown. One potential mechanism for alteration of the microbiota is through diet and nutrition. Previous studies have shown associations of diet with islet autoimmunity, but a direct contributing factor has yet to be identified. Diet, through introduction of antigens and alteration of the composition and function of the microbiota, may elicit the immune system to produce autoreactive responses that result in the destruction of the beta cells. Here, we review the evidence associating diet induced changes in the intestinal microbiota and their contribution to T1D pathogenesis. We further provide a roadmap for determining the effect of diet and other modifiable factors on the entire microbiota ecosystem, including its impact on both immune and beta cell function, as it relates to T1D. A greater understanding of the complex interactions between the intestinal microbiota and several interacting systems in the body (immune, intestinal integrity and function, metabolism, beta cell function, etc.) may provide scientifically rational approaches to prevent development of T1D and other childhood immune and allergic diseases and biomarkers to evaluate the efficacy of interventions.

scholarly journals Investigation of the progress in the women with gestational diabetes mellitus postpartum

2021 ◽  
pp. 45-51
Author(s):  
Thi To Nhu Phan ◽  
Trung Vinh Hoang
Keyword(s):  
Diabetes Mellitus ◽  
Logistic Regression ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Glucose Intolerance ◽  
Beta Cell Function ◽  
Cell Function ◽  
Postpartum Women ◽  
Matsuda Index ◽  
History Of

Aims: Our aim was to evaluate the uptake of postpartum screening, the prevalence and the risk factors for glucose intolerance in women with a recent history of gestational diabetes mellitus (GDM). Methods: All women with a history of GDM are advised to undergo a 75g oral glucose tolerance test (OGTT) around 6 - 12 weeks postpartum. Indices of insulin sensitivity (the Matsuda index and the reciprocal of the homeostasis model assessment of insulin resistance, HOMA-IR) and an index of beta-cell function, the Insulin Secretion-Sensitivity Index-2 (ISSI-2) were calculated based on the OGTT postpartum. Multivariable logistic regression was used to some factors. Results: Of all women (135) who received an OGTT postpartum, 42.2% (57) had glucose intolerance (11.8% impaired fasting glucose, 24.4% impaired glucose tolerance and 6.0% both impaired fasting and impaired glucose tolerance) and 1.5% (2) had overt diabetes. Compared to women with a normal OGTT postpartum, women with glucose intolerance and diabetes were older (32.5 ± 4.3 vs. 30.8 ± 4.8 years, p = 0.049), were more often obese (34.5% vs. 17.3%, p = 0.023). In the multivariable logistic regression, an EM background [OR = 2.76 (1.15 - 6.62), p = 0.023] and the HbA1c level at the time of the OGTT in pregnancy [OR = 4.78 (1.19 - 19.20), p = 0.028] remained significant predictors for glucose intolerance postpartum. Women with glucose intolerance and diabetes postpartum had a similar insulin sensitivity [Matsuda index 0.656 (0.386 - 1.224) vs. 0.778 (0.532 - 1.067), p = 0.709; HOMA-IR 0.004 (0.002 - 0.009) vs. 0.064 (0.003 - 0.007), p = 0.384] but a lower beta-cell function compared to women with a normal OGTT postpartum, remaining significant after adjustment for confounders [ISSI-2 1.6 (1.2 - 2.1) vs. 1.9 (1.7 - 2.4), p = 0.002]. Conclusions: Glucose intolerance is very frequent in early postpartum in women with GDM these women have an impaired beta-cell function. Nearly one third of women did not attend the scheduled OGTT postpartum and these women have an adverse risk profile. More efforts are needed to engage and stimulate women with GDM to attend the postpartum OGTT.

scholarly journals Decreased TCF7L2 protein levels in type 2 diabetes mellitus correlate with downregulation of GIP- and GLP-1 receptors and impaired beta-cell function

2015 ◽  
Vol 24 (10) ◽  
pp. 3004-3004 ◽  
Author(s):  
L. Shu ◽  
A. V. Matveyenko ◽  
J. Kerr-Conte ◽  
J.-H. Cho ◽  
C. H. S. McIntosh ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Protein Levels
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