JTT-608 controls blood glucose by enhancement of glucose-stimulated insulin secretion in normal and diabetes mellitus rats

1999 ◽  
Vol 367 (1) ◽  
pp. 91-99 ◽  
Author(s):  
Takeshi Ohta ◽  
Noboru Furukawa ◽  
Fumihiko Yonemori ◽  
Korekiyo Wakitani
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Glucose Stimulated Insulin Secretion

scholarly journals L-Tryptophan Suppresses Rise in Blood Glucose and Preserves Insulin Secretion in Type-2 Diabetes Mellitus Rats

2012 ◽  
Vol 58 (6) ◽  
pp. 415-422 ◽  
Author(s):  
Tomoko INUBUSHI ◽  
Norio KAMEMURA ◽  
Masataka ODA ◽  
Jun SAKURAI ◽  
Yutaka NAKAYA ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Secretion ◽  
Blood Glucose

scholarly journals The Effect of Resveratrol on Blood Glucose and Blood Lipids in Rats with Gestational Diabetes Mellitus

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Guanli Zhang ◽  
Xiuli Wang ◽  
Baofeng Ren ◽  
Qiongqiong Zhao ◽  
Fang Zhang
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Treatment Group ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Blood Lipids ◽  
Metformin Hydrochloride ◽  
Tnf Α

Background. Previous studies have reported that resveratrol has various biological effects such as anti-inflammatory, antioxidant, and antitumor. This study aimed to investigate the effects of resveratrol on blood glucose and blood lipids in rats with gestational diabetes mellitus (GDM). Methods. The rat diabetes model was prepared by one-time intraperitoneal injection of streptozotocin (STZ, 35 mg/kg). Fasting blood glucose was measured by using a blood glucose meter. The ELISA method was used to detect the levels of insulin, leptin, adiponectin, resistin, TNF-α, and IL-6. The content of TC, TG, LDL-C, and HDL-C was determined by using an automatic biochemical detector. Results. Compared with the GDM group, the insulin level in the resveratrol (120 and 240 mg/kg) treatment group was significantly increased. But, the blood glucose level and body weight were significantly reduced. The content of TC, TG, and LDL-C in the resveratrol (240 mg/kg) treatment group was significantly reduced, and the content of HDL-C was significantly increased. In addition, leptin, resistin, TNF-α, and IL-6 levels in the 240 mg/kg resveratrol treatment group were significantly reduced, and adiponectin was significantly increased. Also, resveratrol (240 mg/kg) was stronger than metformin hydrochloride in improving insulin secretion and regulating blood lipids and adipokine content. Conclusion. Resveratrol has a dose-dependent effect on GDM rats to increase insulin secretion, reduce blood glucose and body weight, and regulate blood lipids and plasma adipokines.

scholarly journals RIPK2 Dictates Insulin Responses to Tyrosine Kinase Inhibitors in Obese Male Mice

Endocrinology ◽  
2020 ◽  
Vol 161 (8) ◽  
Author(s):  
Brittany M Duggan ◽  
Joseph F Cavallari ◽  
Kevin P Foley ◽  
Nicole G Barra ◽  
Jonathan D Schertzer
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Blood Glucose Control ◽  
Tolerance Test ◽  
Independent Manner ◽  
Glucose Stimulated Insulin Secretion ◽  
Insulin Responses

Abstract Tyrosine kinase inhibitors (TKIs) used in cancer are also being investigated in diabetes. TKIs can improve blood glucose control in diabetic cancer patients, but the specific kinases that alter blood glucose or insulin are not clear. We sought to define the role of Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) in mouse models of insulin resistance. We tested the TKI gefitinib, which inhibits RIPK2 activity, in wild-type (WT), Nod1–/–, Nod2–/–, and Ripk2–/– mice fed an obesogenic high-fat diet. Gefitinib lowered blood glucose during a glucose tolerance test (GTT) in a nucleotide-binding oligomerization domain (NOD)–RIPK2-independent manner in all obese mice. However, gefitinib lowered glucose-stimulated insulin secretion only in obese Ripk2–/– mice. Gefitinib had no effect on insulin secretion in obese WT, Nod1–/–, or Nod2–/– mice. Hence, genetic deletion of Ripk2 promoted the insulin-sensitizing potential of gefitinib, since this TKI lowered both blood glucose and insulin only in Ripk2–/– mice. Gefitinib did not alter the inflammatory profile of pancreas, adipose, liver, or muscle tissues in obese Ripk2–/– mice compared with obese WT mice. We also tested imatinib, a TKI that does not inhibit RIPK2 activity, in obese WT mice. Imatinib lowered blood glucose during a GTT, consistent with TKIs lowering blood glucose independently of RIPK2. However, imatinib increased glucose-stimulated insulin secretion during the glucose challenge. These data show that multiple TKIs lower blood glucose, where actions of TKIs on RIPK2 dictate divergent insulin responses, independent of tissue inflammation. Our data show that RIPK2 limits the insulin sensitizing effect of gefitinib, whereas imatinib increased insulin secretion.

Small molecule glucokinase activators as novel anti-diabetic agents

2005 ◽  
Vol 33 (2) ◽  
pp. 371-374 ◽  
Author(s):  
B. Leighton ◽  
A. Atkinson ◽  
M.P. Coghlan
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Type Ii Diabetes Mellitus ◽  
Glucose Sensing ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Glucokinase Activators

The monomeric enzyme GK (glucokinase) has a low affinity for glucose and, quantitatively, is largely expressed in the liver and pancreatic β-cells, playing a key ‘glucose sensing’ role to regulate hepatic glucose balance and insulin secretion. Mutations of GK in man can be inactivating, to cause a form of diabetes mellitus, or activating, to lower blood glucose levels. Recently, models of GK protein structure have helped to elucidate the role of inactivating and activating mutations, with the latter revealing an allosteric binding site, possibly for an unknown physiological activator. However, this discovery was pre-dated by Drug Discovery projects that have identified small organic molecules that activate pancreatic and liver GK enzyme activity. These compounds stimulate insulin secretion in islets and glucose metabolism in hepatocytes. The profile of these GK activators, both in vitro and in vivo and the potential role that GK activators play in lowering blood glucose levels in Type II diabetes mellitus will be discussed.

Elevated Circulating LINC-P21 Serves as a Diagnostic Biomarker of Type 2 Diabetes Mellitus and Regulates Pancreatic β-cell Function by Sponging miR-766-3p to Upregulate NR3C2

2020 ◽  
Author(s):  
Zhibin Cao ◽  
Fuwang Yao ◽  
Yuqin Lang ◽  
Xueqiang Feng
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Cell Proliferation ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Secretion ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucose Stimulated Insulin Secretion

Abstract Objective The purpose of this study was to evaluate the clinical value and biological function of long non-coding RNA (lncRNA) LINC-P21 in type 2 diabetes mellitus (T2DM), and explore the underlying mechanisms. Methods The expression of LINC-P21 was estimated using quantitative real-time PCR. The functional role of LINC-P21 was explored by gain- and loss-of-function experiments. INS-1 cell proliferation was analyzed using a cell counting kit-8 (CCK-8)assay, and the glucose-stimulated insulin secretion was measured using an ELISA kit. The miRNAs that might be sponged by LINC-P21 were analyzed, and the subsequent target genes were predicted and assessed in INS-1 cells. Results Serum expression of LINC-P21 was elevated in T2DM patients, which was correlated with fasting blood glucose levels and disease diagnosis. The glucose-stimulated insulin secretion and the proliferation of INS-1 cells were enhanced by LINC-P21 knockdown, but the overexpression of LINC-P21 led to opposite effects. miR-766-3p could be directly inhibited by LINC-P21 in INS-1 cells and reverse the effects of LINC-P21 on β-cell function. Additionally, NR3C2 was determined as a target of miR-766-3p, which could be positively regulated by LINC-P21 and had same effects with LINC-P21 on INS-1 cell proliferation and insulin secretion. Conclusion All the data demonstrated that serum elevated LINC-P21 and decreased miR-766-3p serve as candidate diagnostic biomarkers in T2DM patients. LINC-P21 acts as a potential regulator in insulin secretion and proliferation of pancreatic β-cells through targeting miR-766-3p to upregulate NR3C2.

scholarly journals Effect of Trigona honey on Blood glucose levels Diabetes Mellitus In Balb/c Mice

2020 ◽  
Vol 9 (5) ◽  
pp. 314-317
Author(s):  
Tri Damayanty Syamsul ◽  
◽  
Rosdiana Natzir ◽  
Marhaen Hardjo ◽  
Hasyim Kasim ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Daily Intake ◽  
Intervention Group ◽  
Total Phenolic ◽  
Control Group ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Body Tissues

Introduction Diabetes Mellitus (DM) is a multicultural metabolic disease characterized by hyperglycemia due to abnormalities in insulin secretion, insulin action, or both. Abnormalities in insulin secretion or action cause problems in the metabolism of carbohydrates, fats, and proteins. DM Type II is characterized by the occurrence of insulin resistance in body tissues. Trigona honey is rich in phenolic compounds because it is food collected by bees from plants. The total phenolic content in honey is highly correlated with antioxidant activity. In this study, we aimed to see the different effects of trigona honey (Tetragonula sp) on plasma insulin and blood glucose levels in mice with diabetes mellitus. Methods. Balb/c mice (n= 28) were randomly assigned into the control group (n=7), negative control, positive control, and intervention group which received a daily intake of trigona honey (n= 14). Results. showed that administration of trigona honey can increase administration of the metformin. This is caused because honey contains high antioxidants and contains bioactive compounds such as alkaloids, flavonoids, triterpenoids, and phenol compounds. Conclusion. Daily consumption of trigona honey has a remarkable potential to decrease the blood glucose, thus it can contribute to the prevention of the diabetes mellitus development.

scholarly journals A REVIEW ON BASTI CHIKITSA IN PRAMEHA: A CRITICAL ANALYSIS

2021 ◽  
Vol 12 (5) ◽  
pp. 110-114
Author(s):  
Suma K J ◽  
Meghana N ◽  
Shalini C
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Metabolic Disorder ◽  
Critical Analysis ◽  
Insulin Action ◽  
Adult Population ◽  
Main Line ◽  
Daytime Sleep ◽  
Lack Of Exercise

Prameha is a Tridoshaja Vyadhi with Kapha predominance. It is a lifestyle disorder and Charaka explains it as a Santarpana Janya Vyadhi, caused due to overindulgence in heavy and richly nutritious food, daytime sleep, lack of exercise, other sedentary habits and not doing seasonal purification. All these etiological factors are responsible for the formation of Vitiated Meda and Kleda (deliquesce) i.e. Abhishyanda. The disease is mainly characterized by Prabhuta and Avila Mutrata. Prameha can be correlated with Diabetes Mellitus. Diabetes mellitus is a metabolic disorder of multiple aetiology, characterized by an increase in plasma blood glucose resulting from defects in insulin secretion, insulin action, or both. Globally, an estimated 463 million adults are living with Diabetes. Diabetes Currently affects more than 62 million people which is more than 7.1% of India’s adult population. As Prameha is a Santarpana Janya Vyadhi, Apatarpana is the main line of treatment. Charaka explains various Shodhana procedures in Prameha and contraindicates Basti in it, as it will increase the progress of the disease. But still, Acharyas explain various Basti Karmas for Prameha. Hence here is an attempt to critically analyse Basti Karma as a line of treatment in Prameha.

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