Effects of Pterostilbene on Diabetes, Liver Steatosis and Serum Lipids

2020 ◽  
Vol 28 (2) ◽  
pp. 238-252 ◽  
Author(s):  
Saioa Gómez-Zorita ◽  
Iñaki Milton-Laskíbar ◽  
Leixuri Aguirre ◽  
Alfredo Fernández-Quintela ◽  
Jianbo Xiao ◽  
...  

: Pterostilbene, a phenolic compound derived from resveratrol, possesses greater bioavailability than its parent compound due to the presence of two methoxyl groups. In this review, the beneficial effects of pterostilbene on diabetes, liver steatosis and dyslipidemia are summarized. Pterostilbene is a useful bioactive compound in preventing type 1 diabetes, insulin resistance and type 2 diabetes in animal models. Concerning type 1 diabetes, the main mechanisms described to justify the positive effects of this phenolic compound are increased liver glycogen content and hepatic glucokinase and phosphofructokinase activities, the recovery of pancreatic islet architecture, cytoprotection and a decrease in serum and pancreatic pro-inflammatory cytokines. As for type 2 diabetes, increased liver glucokinase and glucose-6-phosphatase and decreased fructose-1,6-biphosphatase activities are reported. When insulin resistance is induced by diets, a greater activation of insulin signaling cascade has been reported, increased cardiotrophin-1 levels and liver glucokinase and glucose- 6-phosphatase activities, and a decreased fructose-1,6-biphosphatase activity. Data concerning pterostilbene and liver steatosis are scarce so far, but the reduction in oxidative stress induced by pterostilbene may be involved since oxidative stress is related to the progression of steatosis to steatohepatitis. Finally, pterostilbene effectively reduces total cholesterol, LDL-cholesterol and serum triglyceride levels, while increases HDL-cholesterol in animal models of dyslipidemia.

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1746-P
Author(s):  
PATTARA WIROMRAT ◽  
MELANIE CREE-GREEN ◽  
BRYAN C. BERGMAN ◽  
KALIE L. TOMMERDAHL ◽  
AMY BAUMGARTNER ◽  
...  

2009 ◽  
Vol 87 (1) ◽  
pp. 37-50 ◽  
Author(s):  
D.B. McNamara ◽  
S.N. Murthy ◽  
A.N. Fonseca ◽  
C.V. Desouza ◽  
P.J. Kadowitz ◽  
...  

Diabetes is a complex disorder characterized by impaired insulin formation, release or action (insulin resistance), elevated blood glucose, and multiple long-term complications. It is a common endocrine disorder of humans and is associated with abnormalities of carbohydrate and lipid metabolism. There are two forms of diabetes, classified as type 1 and type 2. In type 1 diabetes, hyperglycemia is due to an absolute lack of insulin, whereas in type 2 diabetes, hyperglycemia is due to a relative lack of insulin and insulin resistance. More than 90% of people with diabetes have type 2 with varied degrees of insulin resistance. Insulin resistance is often associated with impaired insulin secretion, and hyperglycemia is a common feature in both types of diabetes, but failure to make a distinction between the types of diabetes in different animal models has led to confusion in the literature. This is particularly true in relation to cardiovascular disease in the presence of diabetes and especially the response to vascular injury, in which there are major differences between the two types of diabetes. Animal models do not completely mimic the clinical disease seen in humans. Animal models are at best analogies of the pathologic process they are designed to represent. The focus of this review is an analysis of intimal hyperplasia following catheter-induced vascular injury, including factors that may complicate comparisons between different animal models or between in vitro and in vivo studies. We examine the variables, pitfalls, and caveats that follow from the manner of induction of the injury and the diabetic state of the animal. The efficacy of selected antidiabetic drugs in inhibiting the development of the hyperplastic response is also discussed.


2008 ◽  
Vol 93 (5) ◽  
pp. 1834-1840 ◽  
Author(s):  
Mathis Grossmann ◽  
Merlin C. Thomas ◽  
Sianna Panagiotopoulos ◽  
Ken Sharpe ◽  
Richard J. MacIsaac ◽  
...  

Abstract Context: Low testosterone levels are common in men with type 2 diabetes and may be associated with insulin resistance. Objective: We investigated prevalence of testosterone deficiency and the relationship between testosterone and insulin resistance in a large cohort of men with type 2 and type 1 diabetes. Design: The study was a cross-sectional survey of 580 men with type 2 diabetes and 69 men with type 1 diabetes. A subgroup of 262 men with type 2 diabetes was then reassessed after a median of 6 months. Results: Forty-three percent of men with type 2 diabetes had a reduced total testosterone, and 57% had a reduced calculated free testosterone. Only 7% of men with type 1 diabetes had low total testosterone. By contrast, 20.3% of men with type 1 diabetes had low calculated free testosterone, similar to that observed in type 2 diabetes (age-body mass index adjusted odds ratio = 1.4; 95% confidence interval = 0.7–2.9). Low testosterone levels were independently associated with insulin resistance in men with type 1 diabetes as well as type 2 diabetes. Serial measurements also revealed an inverse relationship between changes in testosterone levels and insulin resistance. Conclusions: Testosterone deficiency is common in men with diabetes, regardless of the type. Testosterone levels are partly influenced by insulin resistance, which may represent an important avenue for intervention, whereas the utility of testosterone replacement remains to be established in prospective trials.


2019 ◽  
Vol 10 ◽  
pp. 204201881986322 ◽  
Author(s):  
Lara E. Graves ◽  
Kim C. Donaghue

Type 1 and type 2 diabetes are increasing in prevalence and diabetes complications are common. Diabetes complications are rarely studied in youth, despite the potential onset in childhood. Microvascular complications of diabetes include retinopathy, diabetic kidney disease or nephropathy, and neuropathy that may be somatic or autonomic. Macrovascular disease is the leading cause of death in patients with type 1 diabetes. Strict glycaemic control will reduce microvascular and macrovascular complications; however, they may still manifest in youth. This article discusses the diagnosis and treatment of complications that arise from type 1 and type 2 diabetes mellitus in youth. Screening for complications is paramount as early intervention improves outcome. Screening should commence from 11 years of age depending on the duration of type 1 diabetes or at diagnosis for patients with type 2 diabetes. Diabetic retinopathy may require invasive treatment such as laser therapy or intravitreal antivascular endothelial growth factor therapy to prevent future blindness. Hypertension and albuminuria may herald diabetic nephropathy and require management with angiotensin converting enzyme (ACE) inhibition. In addition to hypertension, dyslipidaemia must be treated to reduce macrovascular complications. Interventional trials aimed at examining the treatment of diabetes complications in youth are few. Statins, ACE inhibitors and metformin have been successfully trialled in adolescents with type 1 diabetes with positive effects on lipid profile, microalbuminuria and measures of vascular health. Although relatively rare, complications do occur in youth and further research into effective treatment for diabetes complications, particularly therapeutics in children in addition to prevention strategies is required.


Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 400
Author(s):  
Hitoe Mori ◽  
Hirokazu Takahashi ◽  
Keiichiro Mine ◽  
Ken Higashimoto ◽  
Kanako Inoue ◽  
...  

Accumulating evidence has suggested that viral infection causes type 1 diabetes due to direct β-cell damage and the triggering of autoimmune reactivity to β cells. Here, we elucidated that the tyrosine kinase 2 (Tyk2) gene, encoding an interferon receptor signaling molecule, is responsible for virus-induced diabetes in mice, and its promoter variant confers a risk of type 1 diabetes in humans. This study investigated the relationship between a TYK2 promoter variant (TYK2PV) and insulin secretion in type 2 diabetes patients. TYK2PV status was determined using direct DNA sequencing and its associations with fasting insulin, C-peptide, and homeostatic model assessment of insulin resistance (HOMA-IR) were evaluated in type 2 diabetes patients without sulfonylurea or insulin medication. Of the 172 patients assessed, 18 (10.5%) showed TYK2PV-positivity. Their body mass index (BMI) was significantly lower than in those without the variant (23.4 vs. 25.4 kg/m2, p = 0.025). Fasting insulin (3.9 vs. 6.2 μIU/mL, p = 0.007), C-peptide (1.37 vs. 1.76 ng/mL, p = 0.008), and HOMA-IR (1.39 vs. 2.05, p = 0.006) were lower in those with than in those without the variant. Multivariable analysis identified that TYK2PV was associated with fasting insulin ≤ 5 μIU/mL (odds ratio (OR) 3.63, p = 0.025) and C-peptide ≤ 1.0 ng/mL (OR 3.61, p = 0.028), and also lower insulin resistance (HOMA-IR ≤ 2.5; OR 8.60, p = 0.042). TYK2PV is associated with impaired insulin secretion and low insulin resistance in type 2 diabetes. Type 2 diabetes patients with TYK2PV should be carefully followed in order to receive the appropriate treatment including insulin injections.


2007 ◽  
Vol 293 (6) ◽  
pp. E1687-E1696 ◽  
Author(s):  
Eun-Gyoung Hong ◽  
Dae Young Jung ◽  
Hwi Jin Ko ◽  
Zhiyou Zhang ◽  
Zhexi Ma ◽  
...  

Although insulin resistance has been traditionally associated with type 2 diabetes, recent evidence in humans and animal models indicates that insulin resistance may also develop in type 1 diabetes. A point mutation of insulin 2 gene in Ins2Akita mice leads to pancreatic β-cell apoptosis and hyperglycemia, and these mice are commonly used to investigate type 1 diabetes and complications. Since insulin resistance plays an important role in diabetic complications, we performed hyperinsulinemic-euglycemic clamps in awake Ins2Akita and wild-type mice to measure insulin action and glucose metabolism in vivo. Nonobese Ins2Akita mice developed insulin resistance, as indicated by an ∼80% reduction in glucose infusion rate during clamps. Insulin resistance was due to ∼50% decreases in glucose uptake in skeletal muscle and brown adipose tissue as well as hepatic insulin action. Skeletal muscle insulin resistance was associated with a 40% reduction in total GLUT4 and a threefold increase in PKCε levels in Ins2Akita mice. Chronic phloridzin treatment lowered systemic glucose levels and normalized muscle insulin action, GLUT4 and PKCε levels in Ins2Akita mice, indicating that hyperglycemia plays a role in insulin resistance. Echocardiography showed significant cardiac remodeling with ventricular hypertrophy that was ameliorated following chronic phloridzin treatment in Ins2Akita mice. Overall, we report for the first time that nonobese, insulin-deficient Ins2Akita mice develop type 2 diabetes phenotypes including peripheral and hepatic insulin resistance and cardiac remodeling. Our findings provide important insights into the pathogenesis of metabolic abnormalities and complications affecting type 1 diabetes and lean type 2 diabetes subjects.


2018 ◽  
Vol 27 (6) ◽  
pp. 549-554 ◽  
Author(s):  
Anara Karaca ◽  
Filiz Bakar-Ates ◽  
Nese Ersoz-Gulcelik

Background/Aims: Spexin is a novel peptide which has a potential role as a biomarker of insulin resistance, diabetes, and obesity. Our aim was to measure spexin levels in lean type 1 diabetic patients and its relevance to glycemic parameters without the presence of obesity or insulin resistance. Subjects and Methods: This cross-sectional study included 29 type 1 and 30 type 2 diabetic patients and a control group of 23 healthy subjects with adjusted age, sex, and body mass index (BMI). Height and weight were measured using standard techniques. Glucose levels, triglycerides, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, serum cortisol levels, and spexin levels were measured in each patient. Results: The median fasting serum spexin levels were significantly lower in patients with type 1 and type 2 diabetes than in control subjects (p = 0.008 and p = 0.041, respectively). Spexin levels were not correlated with glycemic parameters, lipids, BMI, cortisol levels, and thyroid-stimulating hormone (p > 0.05). Only age turned out to be correlated with spexin levels in patients with type 1 diabetes when we analyzed the groups separately. Regression models, including age and diabetes duration, revealed no association between age and spexin levels. Regression models, including cortisol, BMI, and HbA1c, revealed no association with spexin levels within each group. Conclusion: The presence of type 1 diabetes is associated with lower spexin levels, independent of glucose, lipid parameters, and BMI. The expression of spexin in the pancreas apart from the current glycemic control of the patients may be the main determinant of spexin levels in type 1 diabetic patients.


Sign in / Sign up

Export Citation Format

Share Document