scholarly journals The Efficacy of Lowering Blood Glucose Levels Using the Extracts of Fermented Bitter Melon in the Diabetic Mice

2015 ◽  
Vol 58 (3) ◽  
pp. 259-265 ◽  
Author(s):  
Hye Seon Park ◽  
Woo Kyeong Kim ◽  
Hyun Pyo Kim ◽  
Young Geol Yoon
Keyword(s):  
Blood Glucose ◽  
Bitter Melon ◽  
Diabetic Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels

scholarly journals Leptin contributes to the beneficial effects of insulin treatment in streptozotocin-diabetic male mice

2018 ◽  
Vol 315 (6) ◽  
pp. E1264-E1273
Author(s):  
Ursula H. Neumann ◽  
Michelle M. Kwon ◽  
Robert K. Baker ◽  
Timothy J. Kieffer
Keyword(s):  
Blood Glucose ◽  
Insulin Therapy ◽  
Daily Injection ◽  
Diabetic Mice ◽  
Glucose Lowering ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Lowering Effect ◽  
Blood Glucose Levels ◽  
Glucose Lowering Effect

It was long thought that the only hormone capable of reversing the catabolic consequences of diabetes was insulin. However, various studies have demonstrated that the adipocyte-derived hormone leptin can robustly lower blood glucose levels in rodent models of insulin-deficient diabetes. In addition, it has been suggested that some of the metabolic manifestations of insulin-deficient diabetes are due to hypoleptinemia as opposed to hypoinsulinemia. Because insulin therapy increases leptin levels, we sought to investigate the contribution of leptin to the beneficial effects of insulin therapy. To do this, we tested insulin therapy in streptozotocin (STZ) diabetic mice that were either on an ob/ ob background or that were given a leptin antagonist to determine if blocking leptin action would blunt the glucose-lowering effects of insulin therapy. We found that STZ diabetic ob/ ob mice have a diminished blood glucose-lowering effect in response to insulin therapy compared with STZ diabetic controls and exhibited more severe weight loss post-STZ injection. In addition, STZ diabetic mice administered a leptin antagonist through daily injection or plasmid expression respond less robustly to insulin therapy as assessed by both fasting blood glucose levels and blood glucose levels during an oral glucose tolerance test. However, leptin antagonism did not prevent the insulin-induced reduction in β-hydroxybutyrate and triglyceride levels. Therefore, we conclude that elevated leptin levels can contribute to the glucose-lowering effect of insulin therapy in insulin-deficient diabetes.

scholarly journals Hypoglycemic Activity of Aqueous Extracts fromCatharanthus roseus

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Elisa Vega-Ávila ◽  
José Luis Cano-Velasco ◽  
Francisco J. Alarcón-Aguilar ◽  
María del Carmen Fajardo Ortíz ◽  
Julio César Almanza-Pérez ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Intraperitoneal Administration ◽  
Free Fraction ◽  
Hypoglycemic Activity ◽  
Aqueous Extracts ◽  
Diabetic Mice ◽  
Aqueous Fraction ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Stem Extract

Introduction.Catharanthus roseus(L.) is used in some countries to treat diabetes. The aim of this study was to evaluate the hypoglycemic activity of extracts from the flower, leaf, stem, and root in normal and alloxan-induced diabetic mice.Methods. Roots, leaves, flowers, and stems were separated to obtain organic and aqueous extracts. The blood glucose lowering activity of these extracts was determinate in healthy and alloxan-induced (75 mg/Kg) diabetic mice, after intraperitoneal administration (250 mg/Kg body weight). Blood samples were obtained and blood glucose levels were analyzed employing a glucometer. The data were statistically compared by ANOVA. The most active extract was fractioned. Phytochemical screen and chromatographic studies were also done.Results. The aqueous extracts fromC. roseusreduced the blood glucose of both healthy and diabetic mice. The aqueous stem extract (250 mg/Kg) and its alkaloid-free fraction (300 mg/Kg) significantly () reduced blood glucose in diabetic mice by 52.90 and 51.21%. Their hypoglycemic activity was comparable to tolbutamide (58.1%, ).Conclusions. The best hypoglycemic activity was presented for the aqueous extracts and by alkaloid-free stem aqueous fraction. This fraction is formed by three polyphenols compounds.

scholarly journals Effect of reduced dietary zinc intake on carbohydrate and Zn metabolism in the genetically diabetic mouse (C57BL/KsJ db+/db+)

1988 ◽  
Vol 60 (3) ◽  
pp. 499-507 ◽  
Author(s):  
Susan Southon ◽  
Z. Kechrid ◽  
A. J. A. Wright ◽  
Susan J. Fairweather-Tait
Keyword(s):  
Blood Glucose ◽  
Control Diet ◽  
Fasting Blood Glucose ◽  
Liver Glycogen ◽  
Diabetic Mouse ◽  
Whole Body ◽  
Diabetic Mice ◽  
Control Groups ◽  
Glucose Levels ◽  
Blood Glucose Levels

1. Male, 4–5-week-old, genetically diabetic mice (C57BL/KsJ db/db) and non-diabetic heterozygote litter-mates (C57BL/KsJ db/+)were fed on a diet containing 1 mg zinc/kg (low-Zn groups) or 54 mg Zn/kg (control groups) for 27 d. Food intakes and body-weight gain were recorded regularly. On day 28, after an overnight fast, animals were killed and blood glucose and insulin concentrations, liver glycogen, and femur and pancreatic Zn concentrations were determined.2. The consumption of the low-Zn diet had only a minimal effect on the Zn status of the mice as indicated by growth rate, food intake and femur and pancreatic Zn concentrations. In fact, diabetic mice fed on the low-Zn diet had a higher total food intake than those fed on the control diet. The low-Zn diabetic mice had higher fasting blood glucose and liver glycogen levels than their control counterparts. Fasting blood insulin concentration was unaffected by dietary regimen.3. A second experiment was performed in which the rate of loss of 65Zn, injected subcutaneously, was measured by whole-body counting in the two mouse genotypes over a 28 d period, from 4 to 5 weeks of age. The influence of feeding low-Zn or control diets was also examined. At the end of the study femur and pancreatic Zn and non-fasting blood glucose levels were determined.4. All mice fed on the low-Zn diet showed a marked reduction in whole-body 65Zn loss compared with those animals fed on the control diet. In the low-Zn groups, the loss of 65Zn from the diabetic mice was significantly greater than that from heterozygote mice. This difference was not observed in the control groups. Blood glucose levels were elevated in the low-Zn groups. Possible reasons for these observations are discussed.5. The present study demonstrates an adverse effect of reduced dietary Zn intake on glucose utilization in the genetically diabetic mouse, which occurred before any significant tissue Zn depletion became apparent.

scholarly journals Cadmium Exposure Decreases Fasting Blood Glucose Levels and Exacerbates Type-2 Diabetes in a Mouse Model

2021 ◽  
Author(s):  
Mengyang Li ◽  
Shuai Wang ◽  
Xiuxiu Liu ◽  
Zhijie Sheng ◽  
Bingyan Li ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Fasting Blood Glucose ◽  
Diabetic Group ◽  
Diabetic Mice ◽  
Hepatic Enzymes ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Cd Exposure

Abstract Purpose Although the effects of cadmium (Cd) on the development of diabetes have been extensively investigated, the relationship between Cd exposure and the severity of established diabetes is unclear. Herein, we investigate the effects of long-term exposure to Cd in a streptozotocin-induced mouse model of type 2 diabetes and the underlying mechanism. Methods C57BL/6 Mice were divided into the following four groups: 1) control group; 2) Cd-exposed group; 3) diabetic group; 4) Cd-exposed diabetic group. Cd exposure was established by the administration of 155 ppm CdCl2 in drinking water. After 25 weeks of treatment, serum fasting glucose and insulin were measured. Meanwhile, the liver and pancreas specimens were sectioned and stained with Hematoxylin and eosin. Gluconeogenesis, glycolysis, lactate concentration and fibrosis in liver were evaluated. Results Clinical signs attributable to diabetes were more apparent in Cd-exposed diabetic mice. Interestingly, Cd exposure significantly decreased fasting blood glucose levels in diabetic group. We further demonstrated that the glycolysis related hepatic enzymes, pyruvate kinase M2 (PKM-2) and lactic dehydrogenase A (LDHA) were both increased, while the gluconeogenesis related hepatic enzymes, phosphoenolpyruvate-1 (PCK-1) and glucose-6-phosphatase (G6Pase) were both decreased in Cd exposed diabetic mice, indicating that Cd increased glycolysis and inhibited gluconeogenesis in diabetic model. Moreover, lactate accumulation was noted accompanied by the increased inflammation and fibrosis in the livers of diabetic mice following Cd exposure. Conclusions Cd exposure disturbed glucose metabolism and exacerbated diabetes, providing a biological relevance that DM patients are at greater risk when exposed to Cd.

scholarly journals Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

2019 ◽  
Vol 20 (15) ◽  
pp. 3782 ◽  
Author(s):  
Nobutomo Ikarashi ◽  
Nanaho Mizukami ◽  
Risako Kon ◽  
Miho Kaneko ◽  
Ryogo Uchino ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Water Transport ◽  
Diabetic Mouse ◽  
Diabetic Patients ◽  
Diabetic Mice ◽  
Aquaporin 3 ◽  
Expression Levels ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Site Binding

Xeroderma is a frequent complication in diabetic patients. In this study, we investigated the mechanism underlying the onset of diabetic xeroderma, focusing on aquaporin-3 (AQP3), which plays an important role in water transport in the skin. Dermal water content in diabetic mice was significantly lower than that in control mice. The expression level of AQP3 in the skin was significantly lower in diabetic mice than in control mice. One week after streptozotocin (STZ) treatment, despite their increased blood glucose levels, mice showed no changes in the expression levels of AQP3, Bmal1, Clock, and D site-binding protein (Dbp) in the skin and 8-hydroxydeoxyguanosine (8-OHdG) in the urine. In contrast, two weeks after STZ treatment, mice showed increases in the blood glucose level, decreases in AQP3, Bmal1, Clock, and Dbp levels, and increases in the urinary levels of 8-OHdG. The results of this study suggest that skin AQP3 expression decreases in diabetes, which may limit water transport from the vessel side to the corneum side, causing dry skin. In addition, in diabetic mice, increased oxidative stress triggered decreases in the expression levels of Bmal1 and Clock in the skin, thereby inhibiting the transcription of Aqp3 by Dbp, which resulted in decreased AQP3 expression.

Antidiabetic Activity of Peperomia pellucida In Streptozotocin-Induced Diabetic Mice

2021 ◽  
Vol 7 (2) ◽  
pp. 120-129
Author(s):  
Sholihatil Hidayati
Keyword(s):  
Blood Glucose ◽  
Ethanol Extract ◽  
Hexane Fraction ◽  
Antidiabetic Activity ◽  
Diabetic Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Potential Development ◽  
Lower Blood ◽  
Development Objectives

Background: Diabetes mellitus is a heterogeneous group of diseases in the form of disorders in the body's metabolism clinically. Peperomia pellucida herbs have phytochemical containing which is antidiabetic potential development. Objectives: This study was conducted to compare the antidiabetic activity of ethanol extract and n-hexane fraction of Peperomia pellucida. Material and Methods: This research was conducted by make diabetic mice with 50 mg/kg.bw of streptozotocin induction, which was then treated with ethanol extract and n-hexane fraction of Peperomia pellucida with doses 250 mg/kgbw for 7 days.  Results: The results showed that the ethanol extract and n-hexane fraction of Peperomia pellucida reduced blood glucose levels in diabetic mice due to streptozotocin induction. The n-hexane fraction of Peperomia pellucida can lower blood glucose levels as much 244.00 ± 18.99 mg/dL better than the ethanol extract, which is 99.50 ± 28.17 mg/dL. Conclusions: Peperomia pellucida herb has the potential to be developed as an antidiabetic agent.

Inhibition of Foxo1 function is associated with improved fasting glycemia in diabetic mice

2003 ◽  
Vol 285 (4) ◽  
pp. E718-E728 ◽  
Author(s):  
Jennifer Altomonte ◽  
Anja Richter ◽  
Sonal Harbaran ◽  
Jenny Suriawinata ◽  
Jun Nakae ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Cultured Cells ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Diabetic Mice ◽  
Hepatic Expression ◽  
Glucose Levels ◽  
Fasting Glycemia ◽  
Blood Glucose Levels ◽  
Hepatic Glucose

Excessive hepatic glucose production is a contributing factor to fasting hyperglycemia in diabetes. Insulin suppresses hepatic glucose production by inhibiting the expression of two gluconeogenic enzymes, phospho enolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G-6-Pase). The forkhead transcription factor Foxo1 has been implicated as a mediator of insulin action in regulating hepatic gluconeogenesis, and a Foxo1 mutant (Foxo1-Δ256), devoid of its carboxyl domain, has been shown to interfere with Foxo1 function and inhibit gluconeogenic gene expression in cultured cells. To study the effect of Foxo1-Δ256 on glucose metabolism in animals, the Foxo1-Δ256 cDNA was delivered to the livers of mice by adenovirus-mediated gene transfer. Hepatic Foxo1-Δ256 production resulted in inhibition of gluconeogenic activity, as evidenced by reduced PEPCK and G-6-Pase expression in the liver. Mice treated with the Foxo1-Δ256 vector exhibited significantly reduced blood glucose levels. In contrast, blood glucose levels in control vector-treated animals remained unchanged, which coincided with the lack of alterations in the expression levels of PEPCK and G-6-Pase. When tested in diabetic db/db mice, hepatic production of Foxo1-Δ256 was shown to reduce fasting hyperglycemia. Furthermore, we showed that hepatic Foxo1 expression was deregulated as a result of insulin resistance in diabetic mice and that Foxo1-Δ256 interfered with Foxo1 function via competitive binding to target promoters. These results demonstrated that functional inhibition of Foxo1, caused by hepatic expression of its mutant, is associated with reduced hepatic gluconeogenic activity and improved fasting glycemia in diabetic mice.

scholarly journals Characterization of Alginate from Sargassum duplicatum and the Antioxidant Effect of Alginate–Okra Fruit Extracts Combination for Wound Healing on Diabetic Mice

2020 ◽  
Vol 10 (17) ◽  
pp. 6082
Author(s):  
Zulfa Nailul Ilmi ◽  
Pugar Arga Cristina Wulandari ◽  
Saikhu Akhmad Husen ◽  
Dwi Winarni ◽  
Mochammad Amin Alamsjah ◽  
...  
Keyword(s):  
Wound Healing ◽  
Blood Glucose ◽  
1H Nmr ◽  
Healing Process ◽  
Size Exclusion ◽  
Proton Nuclear Magnetic Resonance ◽  
Diabetic Mice ◽  
High Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels

Diabetes mellitus is a group of metabolic disorders characterized by high blood-glucose levels over a prolonged period that causes complications when an open wound is present. Alginate is an antioxidant and a good absorbent of exudates. Okra fruit contains flavonoids that can act as antioxidants. The antioxidant properties of extracts combination reduce blood-glucose levels significantly to accelerate the activities of wound-healing processes on diabetic mice. Alginate was characterized by Size Exclusion Chromatography-Multiple Angle Laser Light Scattering (SEC-MALLS), thermal stability and Proton Nuclear Magnetic Resonance (1H-NMR). The evaluation of wound healing on 36 male mice were divided into 12 groups including normal control (NC), diabetics control (DC), alginate (DA) and alginate–okra (DAO) groups in three different times by histopathology test on skin tissue. The results of SEC-MALLS analysis showed that alginate as single and homogeneous polysaccharide. The 1H-NMR spectrum showed that the mannuronate/guluronate ratio of the used alginate was 0.91. Alginate, okra fruit extract and their combination were classified as moderate and strong antioxidants. The numbers of fibrocytes, fibroblasts, collagen densities had significantly increased from three to seven days. In contrast, wound width, neutrophil, macrophages had significantly decreased at 14 days. The administration of extracts combination increased the re-epithelization of the wound area and wound-healing process on diabetic mice.

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