scholarly journals A Narrative Review of Human Clinical Trials on the Impact of Phenolic-Rich Plant Extracts on Prediabetes and Its Subgroups

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3733
Author(s):  
Wen Xin Janice Lim ◽  
Cheryl S. Gammon ◽  
Pamela von von Hurst ◽  
Lynne Chepulis ◽  
Rachel A. Page

Phenolic-rich plant extracts have been demonstrated to improve glycemic control in individuals with prediabetes. However, there is increasing evidence that people with prediabetes are not a homogeneous group but exhibit different glycemic profiles leading to the existence of prediabetes subgroups. Prediabetes subgroups have been identified as: isolated impaired fasting glucose (IFG), isolated impaired glucose tolerance (IGT), and combined impaired fasting glucose and glucose intolerance (IFG/IGT). The present review investigates human clinical trials examining the hypoglycemic potential of phenolic-rich plant extracts in prediabetes and prediabetes subgroups. Artemisia princeps Pampanini, soy (Glycine max (L.) Merrill) leaf and Citrus junos Tanaka peel have been demonstrated to improve fasting glycemia and thus may be more useful for individuals with IFG with increasing hepatic insulin resistance. In contrast, white mulberry (Morus alba Linn.) leaf, persimmon (Diospyros kaki) leaf and Acacia. Mearnsii bark were shown to improve postprandial glycemia and hence may be preferably beneficial for individuals with IGT with increasing muscle insulin resistance. Elaeis guineensis leaf was observed to improve both fasting and postprandial glycemic measures depending on the dose. Current evidence remains scarce regarding the impact of the plant extracts on glycemic control in prediabetes subgroups and therefore warrants further study.

2014 ◽  
Vol 11 (4) ◽  
pp. 831-837 ◽  
Author(s):  
Paul A. McAuley ◽  
Haiying Chen ◽  
Duck-chul Lee ◽  
Enrique Garcia Artero ◽  
David A. Bluemke ◽  
...  

Background:The influence of higher physical activity on the relationship between adiposity and cardiometabolic risk is not completely understood.Methods:Between 2000–2002, data were collected on 6795 Multi-Ethnic Study of Atherosclerosis (MESA) participants. Self-reported intentional physical activity in the lowest quartile (0–105 MET-minutes/week) was categorized as inactive and the upper three quartiles (123–37,260 MET-minutes/week) as active. Associations of body mass index (BMI) and waist circumference categories, stratified by physical activity status (inactive or active) with cardiometabolic risk factors (dyslipidemia, hypertension, upper quartile of homeostasis model assessment of insulin resistance [HOMA-IR] for population, and impaired fasting glucose or diabetes) were assessed using logistic regression analysis adjusting for age, gender, race/ethnicity, and current smoking.Results:Among obese participants, those who were physically active had reduced odds of insulin resistance (47% lower; P < .001) and impaired fasting glucose/diabetes (23% lower; P = .04). These associations were weaker for central obesity. However, among participants with a normal waist circumference, those who were inactive were 63% more likely to have insulin resistance (OR [95% CI] 1.63 [1.24–2.15]) compared with the active reference group.Conclusions:Physical activity was inversely related to the cardiometabolic risk associated with obesity and central obesity.


2009 ◽  
Vol 63 (9) ◽  
pp. 1308-1313 ◽  
Author(s):  
M. S. Kostapanos ◽  
H. J. Milionis ◽  
A.-D. Agouridis ◽  
C. V. Rizos ◽  
M. S. Elisaf

2018 ◽  
Vol 115 (38) ◽  
pp. E8996-E9005 ◽  
Author(s):  
Brandon M. Gassaway ◽  
Max C. Petersen ◽  
Yulia V. Surovtseva ◽  
Karl W. Barber ◽  
Joshua B. Sheetz ◽  
...  

Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C ε (PKCε), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high-fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCε protects against high-fat diet-induced hepatic insulin resistance. Here, we employed a systems-level approach to uncover additional signaling pathways involved in high-fat diet-induced hepatic insulin resistance. We used quantitative phosphoproteomics to map global in vivo changes in hepatic protein phosphorylation in chow-fed, high-fat–fed, and high-fat–fed with PKCε knockdown rats to distinguish the impact of lipid- and PKCε-induced protein phosphorylation. This was followed by a functional siRNA-based screen to determine which dynamically regulated phosphoproteins may be involved in canonical insulin signaling. Direct PKCε substrates were identified by motif analysis of phosphoproteomics data and validated using a large-scale in vitro kinase assay. These substrates included the p70S6K substrates RPS6 and IRS1, which suggested cross talk between PKCε and p70S6K in high-fat diet-induced hepatic insulin resistance. These results identify an expanded set of proteins through which PKCε may drive high-fat diet-induced hepatic insulin resistance that may direct new therapeutic approaches for T2D.


2016 ◽  
Vol 32 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Ashish Agarwal ◽  
Anupama Hegde ◽  
Charu Yadav ◽  
Afzal Ahmad ◽  
Poornima Ajay Manjrekar ◽  
...  

2014 ◽  
Vol 12 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Kamran Bagheri Lankarani ◽  
◽  
Ahad Eshraghian ◽  
Saman Nikeghbalian ◽  
Parisa Janghorban ◽  
...  

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