Recovery of β-Cell Functions with Low-Dose Insulin Therapy: Study in Newly Diagnosed Type 2 Diabetes Mellitus Patients

2011 ◽  
Vol 13 (4) ◽  
pp. 461-465 ◽  
Author(s):  
Saptarshi Bhattacharya ◽  
Ariachery C. Ammini ◽  
Viveka Jyotsna ◽  
Nandita Gupta ◽  
Sadanand Dwivedi
2016 ◽  
Vol 101 (2) ◽  
pp. 572-580 ◽  
Author(s):  
Sharmistha Roy Chowdhury ◽  
Rebecca L. Thomas ◽  
Gareth J. Dunseath ◽  
Rajesh Peter ◽  
D. Aled Rees ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1837 ◽  
Author(s):  
Francesca Pivari ◽  
Alessandra Mingione ◽  
Caterina Brasacchio ◽  
Laura Soldati

Type 2 diabetes mellitus (T2DM) is an ensemble of metabolic diseases that has reached pandemic dimensions all over the world. The multifactorial nature of the pathology makes patient management, which includes lifelong drug therapy and lifestyle modification, extremely challenging. It is well known that T2DM is a preventable disease, therefore lowering the incidence of new T2DM cases could be a key strategy to reduce the global impact of diabetes. Currently, there is growing evidence on the efficacy of the use of medicinal plants supplements for T2DM prevention and management. Among these medicinal plants, curcumin is gaining a growing interest in the scientific community. Curcumin is a bioactive molecule present in the rhizome of the Curcuma longa plant, also known as turmeric. Curcumin has different pharmacological and biological effects that have been described by both in vitro and in vivo studies, and include antioxidant, cardio-protective, anti-inflammatory, anti-microbial, nephro-protective, anti-neoplastic, hepato-protective, immunomodulatory, hypoglycaemic and anti-rheumatic effects. In animal models, curcumin extract delays diabetes development, improves β-cell functions, prevents β-cell death, and decreases insulin resistance. The present review focuses on pre-clinical and clinical trials on curcumin supplementation in T2DM and discusses the peculiar mechanisms by which curcumin might ameliorate diabetes management.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Madhuri Patil ◽  
Uma Gunasekaran

Abstract In patients with type 2 diabetes mellitus (T2DM), dysfunction of β-cells starts years before the diagnosis of T2DM and rapidly worsens after overt hyperglycemia. Use of short-term intensive insulin therapy (STIIT) at the time of diagnosis of overt hyperglycemia has shown clinical recovery of β-cells for up to 2 years. A systematic literature review of studies looking for the effect of STIIT, used within two years of diagnosis of T2DM, on the duration from relapse of hyperglycemia to eventual insulin dependence is presented in this abstract. The key phrases ‘type 2 diabetes mellitus’, ‘short-term insulin therapy’, ‘β-cell failure’, and ‘permanent insulin dependence’ were used to search English literature. For simplicity the duration of diabetes in these studies was divided into three periods: Period 1- Diagnosis of T2DM to initiation of STIIT, Period 2- End of STIIT until relapse of hyperglycemia i.e. total glycemic remission period, and Period 3- Relapse of hyperglycemia to permanent dependence on insulin therapy. Studies were excluded if all of their participants had diagnosis of T2DM for more than 2 years at the time of inclusion, i.e., if period 1 was more than 2 years. Six clinical trials involving STIIT were identified (Period 2). No studies that examined the clinical course of T2DM in their patients beyond the relapse of hyperglycemia (Period 3) were identified. This literature review identified a lack of data about this important clinical question- do ‘recovered’ β-cells from STIIT exhibit a better response to non-insulin therapies after the end of period 2 and, hence, delay the secondary β-cell failure in period 3? There is a need to conduct studies with longer follow up to characterize the differences in the disease course between patients treated with STIIT and patients treated with non-insulin therapies. This can help us understand scope of STIIT beyond the initial functional remission of β-cells.


2020 ◽  
Vol 70 (12) ◽  
pp. 4217-4223 ◽  

When discussing insulin resistance and insulin sensitivity, data from literature focuses on obese and overweight patients. In our study on, 110 patients with normal body-mass index with newly diagnosed type 2 diabetes mellitus, with the help of glucose tolerance test, we explored insulin resistance, sensitivity, early insulin secretion and β-cell function assessed by using the following indexes: HOMA-IR, ISI, IGI and HOMA-β. We compared the results from our reference group with a control group of 109 overweight patients with newly diagnosed type 2 diabetes mellitus. Normal weight patients had a statistically significant lower HOMA-IR index than overweight patients (2.65 vs. 3.55, p<0.01), however in both groups HOMA-IR was above the cut-off value of 2.5. HOMA-β was statistically significant lower in normal weight patients than in overweight patients (55.08 vs 65.36, p<0.01). ISI index was in an inverse proportional relationship with HOMA-IR, statistically significant higher in normal weight individuals (5.97 vs.3.48, p<0.01). IGI index was not statistically significant lower in normal weight patients (3.63 vs.3.95, p=0.07). It is important to observe that although they have a normal BMI these patients are insulin-resistant confirming the hypothesis of metabolic obese normal weight patients that develop type 2 diabetes mellitus. The indexes that correlate with HbA1c in normal weight patients, predicting glucose status, are HOMA-β (negative correlation), ISI (positive correlation) and IGI index (negative correlation). Keywords: insulin, β-cell, glycated hemoglobin, type 2 diabetes mellitus


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