scholarly journals Sorbitol increases muscle glucose uptake ex vivo and inhibits intestinal glucose absorption ex vivo and in normal and type 2 diabetic rats

2017 ◽  
Vol 42 (4) ◽  
pp. 377-383 ◽  
Author(s):  
Chika Ifeanyi Chukwuma ◽  
Md. Shahidul Islam
Keyword(s):  
Glycemic Control ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Dependent Manner ◽  
Intestinal Glucose Absorption ◽  
Type 2 Diabetic ◽  
Isolated Rat

Previous studies have suggested that sorbitol, a known polyol sweetener, possesses glycemic control potentials. However, the effect of sorbitol on intestinal glucose absorption and muscle glucose uptake still remains elusive. The present study investigated the effects of sorbitol on intestinal glucose absorption and muscle glucose uptake as possible anti-hyperglycemic or glycemic control potentials using ex vivo and in vivo experimental models. Sorbitol (2.5% to 20%) inhibited glucose absorption in isolated rat jejuna (IC50= 14.6% ± 4.6%) and increased glucose uptake in isolated rat psoas muscle with (GU50= 3.5% ± 1.6%) or without insulin (GU50= 7.0% ± 0.5%) in a concentration-dependent manner. Furthermore, sorbitol significantly delayed gastric emptying, accelerated digesta transit, inhibited intestinal glucose absorption, and reduced blood glucose increase in both normoglycemic and type 2 diabetic rats after 1 h of coingestion with glucose. Data of this study suggest that sorbitol exhibited anti-hyperglycemic potentials, possibly via increasing muscle glucose uptake ex vivo and reducing intestinal glucose absorption in normal and type 2 diabetic rats. Hence, sorbitol may be further investigated as a possible anti-hyperglycemic sweetener.

D-mannitol modulates glucose uptake ex vivo; suppresses intestinal glucose absorption in normal and type 2 diabetic rats

2019 ◽  
Vol 29 ◽  
pp. 30-36 ◽  
Author(s):  
Chika Ifeanyi Chukwuma ◽  
Motlalepula Gilbert Matsabisa ◽  
Ochuko L. Erukainure ◽  
Collins U. Ibeji ◽  
Md. Shahidul Islam
Keyword(s):  
Glucose Uptake ◽  
Ex Vivo ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
Intestinal Glucose Absorption ◽  
Type 2 Diabetic

Antidiabetic with antilipidemic and antioxidant effects of flindersine by enhanced glucose uptake through GLUT4 translocation and PPARγ agonism in type 2 diabetic rats

2021 ◽  
pp. 114883
Author(s):  
Santiagu Stephen Irudayaraj ◽  
Jacob Jincy ◽  
Christudas Sunil ◽  
Veeramuthu Duraipandiyan ◽  
Savarimuthu Ignacimuthu ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Diabetic Rats ◽  
Glut4 Translocation ◽  
Antioxidant Effects ◽  
Type 2 Diabetic

scholarly journals Ethanolic Extract ofButea monospermaLeaves Elevate Blood Insulin Level in Type 2 Diabetic Rats, Stimulate Insulin Secretion in Isolated Rat Islets, and Enhance Hepatic Glycogen Formation

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mehdi Bin Samad ◽  
Ashraf Ul Kabir ◽  
Ninadh Malrina D'Costa ◽  
Farjana Akhter ◽  
Arif Ahmed ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Hepatic Glycogen ◽  
Antihyperglycemic Activity ◽  
Isolated Rat Islets ◽  
Type 2 Diabetic ◽  
Glycogen Formation ◽  
Isolated Rat

We measured a vast range of parameters, in an attempt to further elucidate previously claimed antihyperglycemic activity ofButea monosperma. Our study clearly negates the possibility of antidiabetic activity by inhibited gastrointestinal enzyme action or by reduced glucose absorption. Reduction of fasting and postprandial glucose level was reconfirmed (P<0.05). Improved serum lipid profile via reduced low density lipoprotein (LDL), cholesterol, triglycerides (TG), and increased high density lipoprotein (HDL) was also reestablished (P<0.05). Significant insulin secretagogue activity ofB. monospermawas found in serum insulin assay ofB. monospermatreated type 2 diabetic rats (P<0.01). This was further ascertained by our study on insulin secretion on isolated rat islets (P<0.05). Improved sensitivity of glucose was shown by the significant increase in hepatic glycogen deposition (P<0.05). Hence, we concluded that antihyperglycemic activity ofB. monospermawas mediated by enhanced insulin secretion and enhanced glycogen formation in the liver.

Effect of combination of chlorella intake and aerobic exercise training on glycemic control in type 2 diabetic rats

Nutrition ◽  
2019 ◽  
Vol 63-64 ◽  
pp. 45-50 ◽  
Author(s):  
Naoki Horii ◽  
Natsuki Hasegawa ◽  
Shumpei Fujie ◽  
Masataka Uchida ◽  
Keiko Iemitsu ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Type 2 Diabetic

Boerhaavia diffusa inhibits key enzymes linked to type 2 diabetes in vitro and in silico; and modulates abdominal glucose absorption and muscle glucose uptake ex vivo

2018 ◽  
Vol 106 ◽  
pp. 1116-1125 ◽  
Author(s):  
Olajumoke A. Oyebode ◽  
Ochuko L. Erukainure ◽  
Chika I. Chukwuma ◽  
Collins U. Ibeji ◽  
Neil A. Koorbanally ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Uptake ◽  
In Silico ◽  
Ex Vivo ◽  
Glucose Absorption ◽  
Key Enzymes ◽  
Boerhaavia Diffusa

Abstract 2436: Acute Metformin Treatment Worsens Short-term Stroke Outcome: Comparison Of Underlying Mechanisms In Control And Type 2 Diabetic Rats

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Weiguo Li ◽  
Connie Chung ◽  
Roshini Prakash ◽  
Dhruv Chawla ◽  
Maribeth Johnson ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Infarct Size ◽  
Glucose Control ◽  
Diabetic Rats ◽  
Metformin Treatment ◽  
Stroke Outcome ◽  
Ampk Activity ◽  
Lactate Levels ◽  
Type 2 Diabetic

Background: Admission hyperglycemia aggravates neurovascular injury and worsens outcome in acute ischemic stroke (AIS). Current stroke guidelines recommend glycemic control as an important therapeutic strategy to prevent cerebrovascular complications. We have previously shown that chronic glucose control with metformin prior to AIS prevents cerebrovascular remodeling, reduces hemorrhagic transformation (HT), and improves neurological outcome. The goal of this study was to test the hypothesis that acute glucose control in diabetes prior to AIS will also provide neurovascular protection and improve functional outcome. Methods: Ten-week-old male control and type 2 diabetic Goto-Kakizaki (GK) rats (n=6-9 each group) were treated with or without metformin (300mg/kg/day in drinking water) for 3 days prior to stroke. Infarct size, edema ratio (% edema/infarct), and HT frequency and severity were evaluated in all groups after 3 hr middle cerebral artery occlusion (MCAO) and 21 hr reperfusion. AMPK activity and lactate levels--biomarkers of ischemic brain metabolism--were also measured. Results: Compared to controls, metformin treatment decreased blood glucose levels in diabetic animals (160.4±36.5 vs. 120.1±31.1 mg/dL, p<0.0001). Metformin treatment decreased edema ratio in GKs (0.90±0.71 vs. 1.55±0.70, p<0.05), but increased infarct size (23.3±17.5 vs. 12.5±9.5%, p<0.05). Untreated diabetic rats had lower composite scores for neurological tests (3.8±2.4 vs. 5.9±1.2, p<0.05), indicating worse outcome. Metformin treatment worsened this deficit in both diabetic and control animals (2.4±1.6 vs. 1.9±1.0, p=0.0008). AMPK activity was increased only in metformin-treated GK rats while lactate levels were increased in both groups (p<0.05). Results are expressed as mean ± SD. Conclusion: Worsening of stroke outcome by acute metformin treatment is associated with increased lactate accumulation in both control and diabetic rats. Increased infarct size in diabetic but not control rats may be due to greater AMPK activation in diabetes. Whether this effect is specific to metformin or general to acute glycemic control needs to be confirmed with other glucose control measures.

scholarly journals Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-κB Signaling Pathway in Type 2 Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Li-ping Han ◽  
Chun-jun Li ◽  
Bei Sun ◽  
Yun Xie ◽  
Yue Guan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Hepatic Tissue ◽  
Control Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Type 2 Diabetic

Immune and inflammatory pathways play a central role in the pathogenesis of diabetic liver injury. Celastrol is a potent immunosuppressive and anti-inflammatory agent. So far, there is no evidence regarding the mechanism of innate immune alterations of celastrol on diabetic liver injury in type 2 diabetic animal models. The present study was aimed at investigating protective effects of celastrol on the liver injury in diabetic rats and at elucidating the possible involved mechanisms. We analyzed the liver histopathological and biochemical changes and the expressions of TLR4 mediated signaling pathway. Compared to the normal control group, diabetic rats were found to have obvious steatohepatitis and proinflammatory cytokine activities were significantly upregulated. Celastrol-treated diabetic rats show reduced hepatic inflammation and macrophages infiltration. The expressions of TLR4, MyD88, NF-κB, and downstream inflammatory factors IL-1βand TNFαin the hepatic tissue of treated rats were downregulated in a dose-dependent manner. We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-κB signaling cascade pathways and its downstream inflammatory effectors.

scholarly journals Resistin and Type 2 Diabetes: Regulation of Resistin Expression by Insulin and Rosiglitazone and the Effects of Recombinant Resistin on Lipid and Glucose Metabolism in Human Differentiated Adipocytes

2003 ◽  
Vol 88 (12) ◽  
pp. 6098-6106 ◽  
Author(s):  
Philip G. McTernan ◽  
FFolliott M. Fisher ◽  
George Valsamakis ◽  
Rajkumar Chetty ◽  
Alison Harte ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Uptake ◽  
Protein Secretion ◽  
In Vitro Studies ◽  
Dependent Manner ◽  
Diabetes Status ◽  
Human Diabetes ◽  
Type 2 Diabetic

Abstract Resistin, an adipocyte secreted factor, has been suggested to link obesity with type 2 diabetes in rodent models, but its relevance to human diabetes remains uncertain. Although previous studies have suggested a role for this adipocytokine as a pathogenic factor, its functional effects, regulation by insulin, and alteration of serum resistin concentration by diabetes status remain to be elucidated. Therefore, the aims of this study were to analyze serum resistin concentrations in type 2 diabetic subjects; to determine the in vitro effects of insulin and rosiglitazone (RSG) on the regulation of resistin, and to examine the functional effects of recombinant human resistin on glucose and lipid metabolism in vitro. Serum concentrations of resistin were analyzed in 45 type 2 diabetic subjects and 34 nondiabetic subjects. Subcutaneous human adipocytes were incubated in vitro with insulin, RSG, and insulin in combination with RSG to examine effects on resistin secretion. Serum resistin was increased by approximately 20% in type 2 diabetic subjects compared with nondiabetic subjects (P = 0.004) correlating with C-reactive protein. No other parameters, including adiposity and fasting insulin levels, correlated with serum resistin in this cohort. However, in vitro, insulin stimulated resistin protein secretion in a concentration-dependent manner in adipocytes [control, 1215 ± 87 pg/ml (mean ± sem); 1 nm insulin, 1414.0 ± 89 pg/ml; 1 μm insulin, 1797 ± 107 pg/ml (P &lt; 0.001)]. RSG (10 nm) reduced the insulin-mediated rise in resistin protein secretion (1 nm insulin plus RSG, 971 ± 35 pg/ml; insulin, 1 μm insulin plus RSG, 1019 ± 28 pg/ml; P &lt; 0.01 vs. insulin alone). Glucose uptake was reduced after treatment with 10 ng/ml recombinant resistin and higher concentrations (P &lt; 0.05). Our in vitro studies demonstrated a small, but significant, reduction in glucose uptake with human recombinant resistin in differentiated preadipocytes. In human abdominal sc adipocytes, RSG blocks the insulin-mediated release of resistin secretion in vitro. In conclusion, elevated serum resistin in human diabetes reflects the subclinical inflammation prevalent in type 2 diabetes. Our in vitro studies suggest a modest effect of resistin in reducing glucose uptake, and suppression of resistin expression may contribute to the insulin-sensitizing and glucose-lowering actions of the thiazolidinediones.

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