Dietary Phloridzin Reduces Blood Glucose Levels and ReversesSglt1Expression in the Small Intestine in Streptozotocin-Induced Diabetic Mice

2009 ◽  
Vol 57 (11) ◽  
pp. 4651-4656 ◽  
Author(s):  
Saeko Masumoto ◽  
Yukari Akimoto ◽  
Hideaki Oike ◽  
Masuko Kobori
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Diabetic Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels

scholarly journals Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2474
Author(s):  
Lyudmila V. Gromova ◽  
Serguei O. Fetissov ◽  
Andrey A. Gruzdkov
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Metabolic Diseases ◽  
Glucose Absorption ◽  
Cellular Mechanisms ◽  
Physiological Conditions ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
New Strategy ◽  
Intestinal Glucose Absorption

The worldwide prevalence of metabolic diseases such as obesity, metabolic syndrome and type 2 diabetes shows an upward trend in recent decades. A characteristic feature of these diseases is hyperglycemia which can be associated with hyperphagia. Absorption of glucose in the small intestine physiologically contributes to the regulation of blood glucose levels, and hence, appears as a putative target for treatment of hyperglycemia. In fact, recent progress in understanding the molecular and cellular mechanisms of glucose absorption in the gut and its reabsorption in the kidney helped to develop a new strategy of diabetes treatment. Changes in blood glucose levels are also involved in regulation of appetite, suggesting that glucose absorption may be relevant to hyperphagia in metabolic diseases. In this review we discuss the mechanisms of glucose absorption in the small intestine in physiological conditions and their alterations in metabolic diseases as well as their relevance to the regulation of appetite. The key role of SGLT1 transporter in intestinal glucose absorption in both physiological conditions and in diabetes was clearly established. We conclude that although inhibition of small intestinal glucose absorption represents a valuable target for the treatment of hyperglycemia, it is not always suitable for the treatment of hyperphagia. In fact, independent regulation of glucose absorption and appetite requires a more complex approach for the treatment of metabolic diseases.

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 Multifaceted interplay among mediators and regulators of intestinal glucose absorption: potential impacts on diabetes research and treatment

2015 ◽  
Vol 309 (11) ◽  
pp. E887-E899 ◽  
Author(s):  
Leo Ka Yu Chan ◽  
Po Sing Leung
Keyword(s):  
Small Intestine ◽  
Blood Glucose ◽  
Critical Role ◽  
Glucose Absorption ◽  
Therapeutic Interventions ◽  
Diabetes Research ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Patients With Diabetes ◽  
Intestinal Glucose Absorption

Glucose is the prominent molecule that characterizes diabetes and, like the vast majority of nutrients in our diet, it is absorbed and enters the bloodstream directly through the small intestine; hence, small intestine physiology impacts blood glucose levels directly. Accordingly, intestinal regulatory modulators represent a promising avenue through which diabetic blood glucose levels might be moderated clinically. Despite the critical role of small intestine in blood glucose homeostasis, most physiological diabetes research has focused on other organs, such as the pancreas, kidney, and liver. We contend that an improved understanding of intestinal regulatory mediators may be fundamental for the development of first-line preventive and therapeutic interventions in patients with diabetes and diabetes-related diseases. This review summarizes the major important intestinal regulatory mediators, discusses how they influence intestinal glucose absorption, and suggests possible candidates for future diabetes research and the development of antidiabetic therapeutic agents.

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 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.

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