Lactobacillus reuteri TISTR 2736 alleviates type 2 diabetes in rats via the hepatic IRS1/PI3K/AKT signaling pathway by mitigating oxidative stress and inflammatory mediators.

Purpose: This study investigated the beneficial effects of Lactobacillus reuteri TISTR 2736 on glucose homeostasis, carbohydrate metabolism, and the underlying mechanisms of its actions in type 2 diabetic (T2D) rats.

Methods: A rat model of T2D was established by a combination of a high-fat diet and streptozotocin. The diabetic rats were treated daily with L.

Antihyperglycemic effect of extra virgin sacha inchi oil in type 2 diabetic rats: Mechanisms involved in pancreatic β-cell function and apoptosis.

Background And Aim: The purpose of the study was to investigate the anti-hyperglycemic effect of extra virgin sacha inchi oil (EVSIO) and its possible mechanisms and actions against pancreatic β-cell death and dysfunction in type 2 diabetic (T2D) rats.

Experimental Procedure: T2D rats were induced with a high-fat diet and low-dose of streptozotocin. The rats were then treated for 5 weeks with EVSIO (0.

Mango (Mangifera indica L.) seed kernel extract suppresses hyperglycemia by modulating pancreatic β cell apoptosis and dysfunction and hepatic glucose metabolism in diabetic rats.

This study investigated the anti-hyperglycemic action of mango seed kernel extract (MKE) and various mechanisms involved in its actions to improve pancreatic β cells and hepatic carbohydrate metabolism in diabetic rats. An intraperitoneal injection of 60 mg/kg of streptozotocin (STZ) followed by 30 consecutive days of treatment with MKE (250, 500, and 1000 mg/kg body weight) was used to establish a study group of diabetic rats. Using liquid chromatography-electrospray ionization-quadrupole time-of-flight mass spectrometry (LC-ESI-QTOF-MS/MS) for identification, 26 chemical compounds were found in MKE and the high-performance liquid chromatography (HPLC) analysis of the MKE also revealed the existence of mangiferin, gallic acid, and quercetin.

Sacha Inchi ( L.) Oil Improves Hepatic Insulin Sensitivity and Glucose Metabolism through Insulin Signaling Pathway in a Rat Model of Type 2 Diabetes.

This study aimed to evaluate the role of sacha inchi oil (SI) in alleviating hepatic insulin resistance and improving glucose metabolism by inhibiting oxidative stress and inflammation in a rat model of type 2 diabetes. This model was established by providing a high-fat diet and streptozotocin to the rats, thereby inducing diabetes. The diabetic rats were treated orally with 0.

Protective role of hesperidin against diabetes induced spleen damage: Mechanism associated with oxidative stress and inflammation.

Diabetes mellitus is a metabolic disease affecting various organs, including the spleen and is characterized by chronic hyperglycemia. Oxidative and inflammatory stress are key mediators in the development of spleen damage caused by diabetes. This study aimed to examine the splenoprotective effect of hesperidin and the mechanisms underlying its capacity to reduce oxidative stress and inflammation-mediated spleen damage in diabetes.

Effects of Cultured on Sexual Performance and Erectile Function in Streptozotocin-Induced Diabetic Male Rats.

(CM), a valuable edible and medicinal fungus, has been used as traditional medicine to treat health conditions, as well as hyposexuality in Asian societies for over a century. Due to the high demand, several artificial cultivation methods have been developed for their biological activities. In this study, CM was cultured on medium that contained white rice and silkworm pupae, and the levels of cordycepin and adenosine, as well as its aphrodisiac effects in diabetes-induced erectile dysfunction (DIED), were evaluated.

Hesperidin ameliorates pancreatic β-cell dysfunction and apoptosis in streptozotocin-induced diabetic rat model.

Aims: The current study was conducted to investigate the potential protective effects of hesperidin and its possible mechanisms of action on pancreatic β-cells in diabetes.

Main Methods: Male Sprague Dawley rats were made diabetic using 65 mg/kg intraperitoneal injection of streptozotocin, and then administered daily with 100 mg/kg of hesperidin over 4 weeks. On conclusion of the experiment, blood and pancreatic tissue were collected to determine the function of β-cells, apoptosis, oxidative stress, ER stress, and inflammation.

Protective effect of wax apple (Syzygium samarangense (Blume) Merr. & L.M. Perry) against streptozotocin-induced pancreatic ß-cell damage in diabetic rats.

The purpose of this study was to investigate the protective properties and mechanisms of wax apple (Syzygium samarangense (Blume)) against streptozotocin (STZ)-induced pancreatic ß-cell apoptosis in diabetic rats. Diabetes was induced by STZ (65 mg/kg; i.p.

PAX4 R192H and P321H polymorphisms in type 2 diabetes and their functional defects.

We have previously identified PAX4 mutations causing MODY9 and a recent genome-wide association study reported a susceptibility locus of type 2 diabetes (T2D) near PAX4. In this study, we aim to investigate the association between PAX4 polymorphisms and T2D in Thai patients and examine functions of PAX4 variant proteins. PAX4 rs2233580 (R192H) and rs712701 (P321H) were genotyped in 746 patients with T2D and 562 healthy normal control subjects by PCR and restriction-fragment length polymorphism method.

Testosterone reduces AGTR1 expression to prevent β-cell and islet apoptosis from glucotoxicity.

Hypogonadism in men is associated with an increased incidence of type 2 diabetes. Supplementation with testosterone has been shown to protect pancreatic β-cell against apoptosis due to toxic substances including streptozotocin and high glucose. One of the pathological mechanisms of glucose-induced pancreatic β-cell apoptosis is the induction of the local rennin-angiotensin-aldosterone system (RAAS).

Estrogen reduces endoplasmic reticulum stress to protect against glucotoxicity induced-pancreatic β-cell death.

Estrogen can improve glucose homeostasis not only in diabetic rodents but also in humans. However, the molecular mechanism by which estrogen prevents pancreatic β-cell death remains unclear. To investigate this issue, INS-1 cells, a rat insulinoma cell line, were cultured in medium with either 11.

Testosterone protects against glucotoxicity-induced apoptosis of pancreatic β-cells (INS-1) and male mouse pancreatic islets.

Male hypogonadism associates with type 2 diabetes, and T can protect pancreatic β-cells from glucotoxicity. However, the protective mechanism is still unclear. This study thus aims to examine the antiapoptotic mechanism of T in pancreatic β cells cultured in high-glucose medium.