Reduced Skeletal Muscle Oxygen Uptake and Reduced  -Cell Function: Two early abnormalities in normal glucose-tolerant offspring of patients with type 2 diabetes

Diabetes Care ◽  
2003 ◽  
Vol 26 (7) ◽  
pp. 2126-2132 ◽  
Author(s):  
C. Thamer ◽  
M. Stumvoll ◽  
A. Niess ◽  
O. Tschritter ◽  
M. Haap ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Oxygen Uptake ◽  
Cell Function ◽  
Muscle Oxygen ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Muscle Oxygen Uptake

Liraglutide Therapy in a Prediabetic State: Rethinking the Evidence

2020 ◽  
Vol 16 (7) ◽  
pp. 699-715 ◽  
Author(s):  
Georgios S. Papaetis
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Current Evidence ◽  
Β Cell ◽  
Prediabetic State ◽  
New Therapeutic Approaches ◽  
Normal Glucose

Background: Prediabetes is defined as a state of glucose metabolism between normal glucose tolerance and type 2 diabetes. Continuous β-cell failure and death are the reasons for the evolution from normal glucose tolerance to prediabetes and finally type 2 diabetes. Introduction: The necessity of new therapeutic approaches in order to prevent or delay the development of type 2 diabetes is obligatory. Liraglutide, a long-acting GLP-1 receptor agonist, has 97% homology for native GLP-1. Identification of the trophic and antiapoptotic properties of liraglutide in preclinical studies, together with evidence of sustained β-cell function longevity during its administration in type 2 diabetes individuals, indicated its earliest possible administration during this disease, or even before its development, so as to postpone or delay its onset. Methods: Pubmed and Google databases have been thoroughly searched and relevant studies were selected. Results: This paper explores the current evidence of liraglutide administration both in humans and animal models with prediabetes. Also, it investigates the safety profile of liraglutide treatment and its future role to postpone or delay the evolution of type 2 diabetes. Conclusion: Liralgutide remains a valuable tool in our therapeutic armamentarium for individuals who are overweight or obese and have prediabetes. Future well designed studies will give valuable information that will help clinicians to stratify individuals who will derive the most benefit from this agent, achieving targeted therapeutic strategies.

scholarly journals Expression Profile of Diabetes-Related Genes Associated with Leukocyte Sirtuin 1 Overexpression in Gestational Diabetes

2018 ◽  
Vol 19 (12) ◽  
pp. 3826 ◽  
Author(s):  
Katarzyna Mac-Marcjanek ◽  
Andrzej Zieleniak ◽  
Monika Zurawska-Klis ◽  
Katarzyna Cypryk ◽  
Lucyna Wozniak ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Sirtuin 1 ◽  
Pcr Array ◽  
Array Analysis ◽  
Sirt1 Expression ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Cellular Pathways

Although compelling evidence indicates that Sirtuin 1 (SIRT1) plays a prominent role in type 2 diabetes, its relationship with gestational diabetes (GDM) remains elusive. This study was aimed at identifying diabetes-related genes and cellular pathways linked to changes of leukocyte SIRT1 expression at the time of GDM diagnosis. For this purpose, 122 GDM patients were screened for leukocyte SIRT1 expression, and two subgroups were distinguished, namely GDM/SIRT1(↑) (n = 30, p < 0.05) and GDM/SIRT1(↔) (n = 92, p > 0.05), with significant and insignificant changes in leukocyte SIRT1 expression compared to a normal glucose tolerant (NGT) group (n = 41), respectively. PCR array analysis identified 11 diabetes-related genes with at least a ± 2-fold difference in expression in GDM/SIRT1(↑) patients (n = 9) vs. NGT controls (n = 7); in addition, significant differences in the expression of four of the six investigated genes were confirmed between the entire GDM/SIRT1(↑) group and the whole NGT group (p < 0.05). Interestingly, of these four genes, only ACLY expression was found to significantly differ between GDM/SIRT1(↑) and GDM/SIRT1(↔). This study demonstrates that under hyperglycemic conditions, leukocyte SIRT1 overexpression is accompanied by an over-abundance of three transcripts and an under-abundance of another; these four govern related metabolism, inflammation, and transport functions, suggesting that such alterations might represent systemic biological adaptations with a unique ACLY under-expression in GDM/SIRT1(↑) women.

β-Cell Function and Insulin Sensitivity in Normal Glucose-Tolerant Subjects Stratified by 1-Hour Plasma Glucose Values

2016 ◽  
Vol 18 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Miranda M. Priya ◽  
Anandakumar Amutha ◽  
T.A. Pramodkumar ◽  
Harish Ranjani ◽  
Saravanan Jebarani ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Cell Function ◽  
Β Cell ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Β Cell Function

Ketosis-Prone Type 2 Diabetes: Effect of Hyperglycemia on β-Cell Function and Skeletal Muscle Insulin Signaling

2007 ◽  
Vol 13 (3) ◽  
pp. 283-290 ◽  
Author(s):  
Guillermo Umpierrez ◽  
Dawn Smiley ◽  
Aidar Gosmanov ◽  
Donald Thomason
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Insulin Signaling ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Dissociation of local and global skeletal muscle oxygen transport metrics in type 2 diabetes

2017 ◽  
Vol 31 (8) ◽  
pp. 1311-1317 ◽  
Author(s):  
P. Mason McClatchey ◽  
Timothy A. Bauer ◽  
Judith G. Regensteiner ◽  
Irene E. Schauer ◽  
Amy G. Huebschmann ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Oxygen Transport ◽  
Muscle Oxygen

scholarly journals Study of phases of insulin secretion in pre-diabetes and newly diagnosed type 2 diabetes mellitus

2016 ◽  
Vol 8 (2) ◽  
pp. 85
Author(s):  
Sabreena Mohtarin ◽  
Md. Matiur Rahman ◽  
Subrata Kumar Biswas ◽  
Forhadul Hoque Mollah ◽  
M. Iqbal Arslan
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Beta Cell Function ◽  
Cell Function ◽  
Insulin Level ◽  
Newly Diagnosed ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Second Phases

<p><strong>Background:</strong> Insulin is released from the pancreas in a biphasic manner in response to arterial glucose concentration. The assumption has been generally made that the 30-minute response reflected first-phase insulin release, whereas the 120-minute response reflected second-phase insulin release.</p><p><strong>Objectives:</strong> The aim of this study was to identify the defect in first and second phases of insulin secretion in pre-diabetes and newly diagnosed T2DM.</p><p><strong>Methods:</strong> This case-control study was conducted in the department of Biochemistry, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka from March 2013 to June 2014. All the study subjects (n = 94) were collected from the one point centre, BSMMU as newly diagnosed T2DM, pre-diabetes and healthy normal glucose tolerant subjects according to fasting plasma glucose and 2 hour plasma glucose status. A total of 32 newly diagnosed T2DM and 32 pre-diabetes were included on the basis of inclusion criteria as cases. Another 30 healthy normal glucose tolerant subjects were emolled as control. Fasting blood samples were collected from study subjects to estimate the plasma glucose and insulin level. Again blood samples were taken for measurement of plasma glucose and insulin level at 30 minute and 120 minute on OGTT.</p><p><strong>Results:</strong> Fasting plasma insulin was significantly higher in pre-diabetes than control and T2DM (p = 0.011). Plasma insulin at 30 minute and 120 minute of OGTT were significantly lower in T2DM than control and pre- diabetes (p = 0.001 &amp; 0.016). The insulin secretion in first and second phases were significantly lower in T2DM patients than controls and pre-diabetes (p = 0.000). Beta-cell function was also significantly lower in T2DM than controls and pre-diabetes (p = 0.000). Median values of HOMA-IR were higher in pre-diabetes (1.68) and T2DM (1.53) than control (1.37), but not statistically significant (p = 0.153). There was significant positive correlation of both phases of insulin secretion with FPI, beta-cell function and insulin resistance in T2DM, pre-diabetes and controls.</p><p><strong>Conclusions:</strong> The study reveals that 1st and 2nd phase insulin secretory defect was detected in T2DM, but in pre-diabetes, we have failed to identify insulin secretory defects in both phases.</p>

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