scholarly journals Effects of Polyphenols on Insulin Resistance

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3135
Author(s):  
Gary Williamson ◽  
Katherine Sheedy

Insulin resistance (IR) is apparent when tissues responsible for clearing glucose from the blood, such as adipose and muscle, do not respond properly to appropriate signals. IR is estimated based on fasting blood glucose and insulin, but some measures also incorporate an oral glucose challenge. Certain (poly)phenols, as supplements or in foods, can improve insulin resistance by several mechanisms including lowering postprandial glucose, modulating glucose transport, affecting insulin signalling pathways, and by protecting against damage to insulin-secreting pancreatic β-cells. As shown by intervention studies on volunteers, the most promising candidates for improving insulin resistance are (−)-epicatechin, (−)-epicatechin-containing foods and anthocyanins. It is possible that quercetin and phenolic acids may also be active, but data from intervention studies are mixed. Longer term and especially dose-response studies on mildly insulin resistant participants are required to establish the extent to which (poly)phenols and (poly)phenol-rich foods may improve insulin resistance in compromised groups.

2012 ◽  
Vol 37 (5) ◽  
pp. 997-1002
Author(s):  
Jose E. Galgani ◽  
Karla Vasquez ◽  
Giannella Leonelli ◽  
Alejandra Espinosa ◽  
Hector Araya ◽  
...  

The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Fifteen healthy, young (24 ± 5 years), nonobese (23 ± 2 kg·m–2), insulin-sensitive (ISI composite = 6.0 ± 1.2) individuals and 14 healthy, young (22 ± 2 years), nonobese (24 ± 2 kg·m–2), insulin-resistant (ISI composite = 2.7 ± 1.1) individuals received a 75 g oral glucose dose. Blood samples were drawn before and for 2 h after glucose ingestion for red blood cell glutathione and serum glucose and insulin concentrations. Glycemia before and after glucose ingestion was similar between groups (p = 0.17), which suggest that hyperinsulinemia compensated impaired insulin sensitivity. Red blood cell total (p = 0.81), reduced (p = 0.79), and oxidized (p = 0.88) glutathione concentrations were similar between groups under fasting and postprandial conditions. However, in response to glucose, increases in total and reduced glutathione concentrations were found at the end of the 2 h assessment period in both groups (p < 0.05). Direct associations between postprandial glucose response and red blood cell total (r = 0.52; p < 0.05) and oxidized (r = 0.61; p = 0.02) glutathione concentrations were observed only in insulin-sensitive subjects. In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions.


2015 ◽  
Vol 308 (8) ◽  
pp. E662-E669 ◽  
Author(s):  
Lisette A. Maddison ◽  
Kaitlin E. Joest ◽  
Ryan M. Kammeyer ◽  
Wenbiao Chen

Insulin resistance creates an environment that promotes β-cell failure and development of diabetes. Understanding the events that lead from insulin resistance to diabetes is necessary for development of effective preventional and interventional strategies, and model systems that reflect the pathophysiology of disease progression are an important component toward this end. We have confirmed that insulin enhances glucose uptake in zebrafish skeletal muscle and have developed a zebrafish model of skeletal muscle insulin resistance using a dominant-negative IGF-IR. These zebrafish exhibit blunted insulin signaling and glucose uptake in the skeletal muscle, confirming insulin resistance. In young animals, we observed an increase in the number of β-cells and normal glucose tolerance that was indicative of compensation for insulin resistance. In older animals, the β-cell mass was reduced to that of control with the appearance of impaired glucose clearance but no elevation in fasting blood glucose. Combined with overnutrition, the insulin-resistant animals have an increased fasting blood glucose compared with the control animals, demonstrating that the β-cells in the insulin-resistant fish are in a vulnerable state. The relatively slow progression from insulin resistance to glucose intolerance in this model system has the potential in the future to test cooperating genes or metabolic conditions that may accelerate the development of diabetes and provide new therapeutic targets.


2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Mario Mancini ◽  
Alice Andreassi ◽  
Michela Salvioni ◽  
Fiore Pelliccione ◽  
Gianna Mantellassi ◽  
...  

Myoinositol and D-chiro inositol, which are inositol isomers, have been shown to possess insulin-mimetic properties and to improve insulin resistance, especially in women with polycystic ovary syndrome. However, it has not been determined if this relationship exists also in children. Based on these previous findings, we hypothesized that inositol could be effective in improving insulin sensitivity in children with insulin resistance. To evaluate this hypothesis, we administered both inositol formulations before carrying out an oral glucose tolerance test (OGTT) in a group of obese insulin-resistant male children with high basal insulin levels and compared the values obtained with an OGTT previously conducted without inositol, in the same group, with unchanged BMI. Our results confirm that myoinositol and D-chiro inositol acutely reduce insulin increase after glucose intake mainly in children with high basal insulin level.


2019 ◽  
Vol 20 (3) ◽  
pp. 727 ◽  
Author(s):  
Hyun-Young Na ◽  
Byung-Cheol Lee

Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.


2007 ◽  
Vol 85 (9) ◽  
pp. 856-864 ◽  
Author(s):  
Anamaria Dascalu ◽  
John L. Sievenpiper ◽  
Alexandra L. Jenkins ◽  
Mark P. Stavro ◽  
Lawrence A. Leiter ◽  
...  

Evidence indicates that the glycemia-lowering effect of American ginseng root may be batch dependent. We therefore evaluated the effect of 5 root batches, representative of Ontario-grown American ginseng, on postprandial glucose and insulin indices. Twelve healthy subjects (5 male, 7 female), mean ± SE age 26.5 ± 2 years, body mass index 23.96 ± 3.41 kg/m2, fasting blood glucose 4.77 ± 0.04 mmol/L, were assigned to consume 9 g of American ginseng from 5 farms (A–E), administered in randomized sequence on 5 separate visits, and a water-control during the 6th and last visit. Treatments were consumed 40 min before a 2-hour 75-gram oral glucose tolerance test. Plasma glucose and insulin were measured at baseline, before, and during the test. Compared with control, batches A and C reduced glucose incremental area under the curve (IAUC) by 35.2% (156 vs. 240 mmol·min/L) and 32.6% (162 vs. 240 mmol·min/L), respectively. Batches A, C, and E reduced incremental peak glucose by 1.3, 1.2, and 1.1 mmol/L, respectively. Batch C reduced the insulin IAUC by 27.7% (15.8 vs. 21.8 nmol·min/L). Effects on glucose and insulin parameters were not different across ginseng treatments. The mean of the 5 ginseng treatments reduced peak postprandial glucose by 1.0 mmol/L, glucose IAUC by 27.7% (173 vs. 240 mmol·min/L), and insulin IAUC by 23.8% (16.6 vs. 21.8 nmol·min/L) relative to control. (All results statistically significant at p < 0.05.) American ginseng decreased postprandial glycemia and insulinemia; however, 40% of the batches did not reduce glycemia with the anticipated magnitude, irrespective of their saponin composition.


2020 ◽  
Author(s):  
Constanza Salinas ◽  
Gabriel Espinosa ◽  
Natalia Morales ◽  
Claudio Henriquez ◽  
Gabriel Moran ◽  
...  

Abstract Background: Obesity and insulin resistance (IR) are conditions of increasing prevalence in populations of equids worldwide. The immune impairment described in metabolic dysfunction status in humans has been extensively reported with minimal data regarding horses. The objective of the study was to evaluate the effect of obesity as an isolated factor and in association with insulin resistance on apoptosis, phagocytosis and oxidative burst activity of neutrophils isolated from peripheral blood of lean and obese adult horses with or without insulin resistance, basally and after induction of hyperglycemia through an oral glucose test. Results: No differences in apoptosis were observed between experimental groups at any time point. Phagocytic capacity was significantly diminished at baseline in the obese-IR group (P<0.05) but increased after stimulation of hyperglycemia (P=0.007). Basal reactive oxygen species production differed significantly (P=0.0001) between the obese-insulin sensitive (IS) and lean-IS or obese-IR groups, and decreased significantly after stimulation of hyperglycemia in the lean-IS and obese-IS groups (P<0.05).Conclusions: Results from this study showed that both metabolic status itself, and acute hyperglycemia, are factors that influence PMNs functionality in horses, specifically phagocytosis and oxidative burst. This indicates the need for close monitoring of immune function in horses with inflammatory disease and concurrent obesity and insulin resistance.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yanan Shi ◽  
Dan Liu ◽  
Jihong Yuan ◽  
Lihui Yan ◽  
Zhenfeng Zhan ◽  
...  

Compound Danshen dripping pills (CDDP) is widely used for the treatment of coronary arteriosclerosis and ischemic heart diseases for decades of years. In our study, we interestingly discovered the effects and mechanism of CDDP on insulin resistance that increase the risk factor of cardiovascular diseases. Effects of CDDP on fasting blood glucose, the insulin tolerance test (ITT), the oral glucose tolerance test (OGTT), hepatic function, and underlying mechanism were analyzed in ob/ob mice. CDDP was found improving the impaired insulin signal sensitivity of ob/ob mice by ameliorating insulin and glucose tolerance, improving hepatic phosphorylation of the insulin receptor substrate-1 on Ser 307 (pIRS1) of ob/ob mice, and restoring hepatic function by decreasing serum ALT and AST, which increased in ob/ob mice serum. Decreasing hepatic phosphorylation of pancreatic ER kinase (PERK) and inositol-requiring enzyme-1 (IRE1) regulating hepatic ER stress in the liver of ob/ob mice were increased by CDDP. Furthermore, CDDP was also found stimulating ob/ob mice hepatic autophagy by increasing the expression of Beclin1 and LC3B, while decreasing P62 expression. Our study discovered an important role of CDDP on improving ob/ob mice insulin resistance and liver function probably through relieving hepatic ER stress and stimulating hepatic autophagy, which would broaden the application value and provide more benefits for treating cardiovascular patients. This trial is registered with NCT01659580.


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Mani Mokou ◽  
Shan Yang ◽  
Bin Zhan ◽  
Shan Geng ◽  
Kejia Li ◽  
...  

Background. Previous studies have suggested that Fetuin-B seems to be a secreted adipokine related to metabolic diseases. However, the results have been inconsistent. Here, our objective is to investigate the changes in circulating Fetuin-B levels in women with polycystic ovary syndrome (PCOS) and analyze the association of Fetuin-B and insulin resistance (IR). Methods. The current study is comprised of a cross-sectional study and a series of interventional studies. Oral glucose tolerance test (OGTT) and euglycemic-hyperinsulinemic clamp (EHC) were engaged to assess glucose tolerance and insulin sensitivity. Serum Fetuin-B levels were determined by ELISA. Results. Serum Fetuin-B and TNF-α levels were markedly increased in women with PCOS compared to healthy women. Circulating Fetuin-B was positively associated with body mass index, waist-to-hip ratio, the percentage of body fat (FAT%), systolic blood pressure, triglyceride, low-density lipoprotein cholesterol, fasting blood glucose, 2 h blood glucose after glucose overload, fasting insulin, 2 h insulin after glucose overload, HOMA-insulin resistance index (HOMA-IR), the area under the curve for insulin (AUCi), AUCg, and TNF-α, while negatively associated with M value and follicular stimulating hormone (FSH). During the EHC, Fetuin-B levels were found to be significantly increased in PCOS women. After a glucose challenge, serum Fetuin-B levels in healthy women were significantly increased. Lipid infusion reduced serum Fetuin-B levels in 30 healthy subjects. After six months of glucagon-like peptide-1 receptor agonist (GLP-1RA) intervention, serum Fetuin-B concentrations in PCOS women markedly decreased following ameliorated IR. Conclusion. Our results indicate that Fetuin-B may be a biomarker of IR in individuals with PCOS. This trial is registered with ChiCTR-IIR-16007901.


Author(s):  
Yoshiro Saito

Abstract Selenoprotein P (SeP; encoded by SELENOP) is selenium (Se)-rich plasma protein that is mainly produced in the liver. SeP functions as a Se-transport protein to deliver Se from the liver to other tissues, such as the brain and testis. The protein plays a pivotal role in Se metabolism and antioxidative defense, and it has been identified as a ‘hepatokine’ that causes insulin resistance in type 2 diabetes. SeP levels are increased in type 2 diabetes patients, and excess SeP impairs insulin signalling, promoting insulin resistance. Furthermore, increased levels of SeP disturb the functioning of pancreatic β cells and inhibit insulin secretion. This review focuses on the biological function of SeP and the molecular mechanisms associated with the adverse effects of excess SeP on pancreatic β cells’ function, particularly with respect to redox reactions. Interactions between the liver and pancreas are also discussed.


2015 ◽  
Vol 224 (3) ◽  
pp. 327-341 ◽  
Author(s):  
Xin-gang Yao ◽  
Xin Xu ◽  
Gai-hong Wang ◽  
Min Lei ◽  
Ling-ling Quan ◽  
...  

Impaired glucose-stimulated insulin secretion (GSIS) and increasing β-cell death are two typical dysfunctions of pancreatic β-cells in individuals that are destined to develop type 2 diabetes, and improvement of β-cell function through GSIS enhancement and/or inhibition of β-cell death is a promising strategy for anti-diabetic therapy. In this study, we discovered that the small molecule, N-(2-benzoylphenyl)-5-bromo-2-thiophenecarboxamide (BBT), was effective in both potentiating GSIS and protecting β-cells from cytokine- or streptozotocin (STZ)-induced cell death. Results of further studies revealed that cAMP/PKA and long-lasting (L-type) voltage-dependent Ca2+ channel/CaMK2 pathways were involved in the action of BBT against GSIS, and that the cAMP/PKA pathway was essential for the protective action of BBT on β-cells. An assay using the model of type 2 diabetic mice induced by high-fat diet combined with STZ (STZ/HFD) demonstrated that BBT administration efficiently restored β-cell functions as indicated by the increased plasma insulin level and decrease in the β-cell loss induced by STZ/HFD. Moreover, the results indicated that BBT treatment decreased fasting blood glucose and HbA1c and improved oral glucose tolerance further highlighting the potential of BBT in anti-hyperglycemia research.


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