scholarly journals Effect of Ishophloroglucin A, A Component of Ishige okamurae, on Glucose Homeostasis in the Pancreas and Muscle of High Fat Diet-Fed Mice

Marine Drugs ◽  
2019 ◽  
Vol 17 (11) ◽  
pp. 608 ◽  
Author(s):  
Hye-Won Yang ◽  
Myeongjoo Son ◽  
Junwon Choi ◽  
Seyeon Oh ◽  
You-Jin Jeon ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Functional Food ◽  
Glucose Transporter ◽  
Fasting Glucose ◽  
High Fat ◽  
Β Cells ◽  
Glucose Levels ◽  
Ishige Okamurae ◽  
Prevention Of Diabetes

Ishophloroglucin A (IPA), a component of Ishige okamurae (IO), was previously evaluated to standardize the antidiabetic potency of IO. However, the potential of IPA as a functional food for diabetes prevention has not yet been evaluated. Here, we investigated if 1.35 mg/kg IPA, which is the equivalent content of IPA in 75 mg/kg IO, improved glucose homeostasis in high-fat diet (HFD)-induced diabetes after 12 weeks of treatment. IPA significantly ameliorated glucose intolerance, reducing fasting glucose levels as well as 2 h glucose levels in HFD mice. In addition, IPA exerted a protective effect on the pancreatic function in HFD mice via pancreatic β-cells and C-peptide. The level of glucose transporter 4 (GLUT4) in the muscles of HFD mice was stimulated by IPA intake. Our results suggested that IPA, which is a component of IO, can improve glucose homeostasis via GLUT4 in the muscles of HFD mice. IO may be used as a functional food for the prevention of diabetes.

scholarly journals SPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice

2019 ◽  
Vol 133 (2) ◽  
pp. 351-365 ◽  
Author(s):  
Catalina Atorrasagasti ◽  
Agostina Onorato ◽  
María L. Gimeno ◽  
Luz Andreone ◽  
Mariana Garcia ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Cell Types ◽  
High Fat ◽  
Metabolic Complications ◽  
Glucose Transporter 2 ◽  
Diabetes In Mice ◽  
Key Factor

Abstract Obesity, metabolic syndrome, and type 2 diabetes, three strongly interrelated diseases, are associated to increased morbidity and mortality worldwide. The pathogenesis of obesity-associated disorders is still under study. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular glycoprotein expressed in many cell types including adipocytes, parenchymal, and non-parenchymal hepatic cells and pancreatic cells. Studies have demonstrated that SPARC inhibits adipogenesis and promotes insulin resistance; in addition, circulating SPARC levels were positively correlated with body mass index in obese individuals. Therefore, SPARC is being proposed as a key factor in the pathogenesis of obesity-associated disorders. The aim of this study is to elucidate the role of SPARC in glucose homeostasis. We show here that SPARC null (SPARC−/−) mice displayed an abnormal insulin-regulated glucose metabolism. SPARC−/− mice presented an increased adipose tissue deposition and an impaired glucose homeostasis as animals aged. In addition, the absence of SPARC worsens high-fat diet-induced diabetes in mice. Interestingly, although SPARC−/− mice on high-fat diet were sensitive to insulin they showed an impaired insulin secretion capacity. Of note, the expression of glucose transporter 2 in islets of SPARC−/− mice was dramatically reduced. The present study provides the first evidence that deleted SPARC expression causes diabetes in mice. Thus, SPARC deficient mice constitute a valuable model for studies concerning obesity and its related metabolic complications, including diabetes.

Compensatory Recovery of Blood Glucose Levels in KKAy Mice Fed a High-Fat Diet: Insulin-Sparing Effects of PACAP Overexpression in β Cells

2012 ◽  
Vol 48 (3) ◽  
pp. 647-653 ◽  
Author(s):  
Yusuke Sakurai ◽  
Hiroaki Inoue ◽  
Norihito Shintani ◽  
Akihiro Arimori ◽  
Ken-ichi Hamagami ◽  
...  
Keyword(s):  
Blood Glucose ◽  
High Fat Diet ◽  
High Fat ◽  
Β Cells ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Kkay Mice

scholarly journals Beet (Beta vulgaris) Improve Blood Glucose and AKT2 Gene Expression in High Fat and Fructose-induced Rats

2021 ◽  
Vol 9 (A) ◽  
pp. 882-886
Author(s):  
M. Windi Dona Fitri ◽  
Arta Farmawati ◽  
Sunarti Sunarti
Keyword(s):  
Gene Expression ◽  
Blood Glucose ◽  
Glucose Homeostasis ◽  
Fasting Glucose ◽  
Saturated Fat ◽  
Diet Group ◽  
Normal Diet ◽  
High Fat ◽  
Glucose Levels ◽  
Before And After

ABSTRACT Background: Diet components significant effects on glucose homeostasis. A diet contains high saturated fat and fructose induces insulin resistance and enhanced blood glucose. In contrast, food containing flavonoids such as beet can improve glucose homeostasis via modulation of gene expression, e.g., AKT2, involving glucose metabolism. Aims: This study were to evaluate the benefit of beet on AKT2 gene expression and fasting glucose. Methods: Twenty wistar male was divided into five groups: Normal were fed a normal diet, group HFFD was given a diet containing high fat and fructose, and three groups (HFB1, HFB2, HFB3) were given a diet containing high fat and fructose for eight weeks and continuous fed beet-contained normal diet for six weeks. The percentage of beet in the diet for each 6%, 9%, and 12%, respectively. Results: The fasting glucose was measured before and after the intervention, whereas the gene expression of AKT2 at skeletal muscle tissue was determined after the intervention. A diet high in fat and fructose increased fasting glucose levels, and a beet-contained diet decreased it. Conclusions: The beet 9% substituted diet can improve glucose homeostasis from the effects of a high fat and fructose diet, and the expression of the AKT2 gene may have a role in the process. Keywords: AKT2, Antioxidant, Beet, Fat, Fructose.

Proper mTORC1 Activity Is Required for Glucose Sensing and Early Adaptation in Human Pancreatic β Cells

2020 ◽  
Author(s):  
Qicheng Ni ◽  
Jiaxi Song ◽  
Yichen Wang ◽  
Jiajun Sun ◽  
Jing Xie ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Fasting Glucose ◽  
Dynamic Change ◽  
Human Islets ◽  
Glucose Sensing ◽  
Β Cells ◽  
Β Cell ◽  
Strong Negative Correlation ◽  
Glucose Levels ◽  
Glucose Transporter 2

Abstract Context The mechanistic target of rapamycin complex I (mTORC1) is crucial for β-cell identity and function in rodents. However, its possible relevance to the physiopathology of diabetes in humans remains unclear. Objective This work aimed to understand the participation of mTORC1 in human β cells in prediabetes and diabetes. Design We evaluated the PS6 immunofluorescence intensity in islets of pancreatic sections from 12 nondiabetic (ND), 11 impaired fasting glucose (IFG), and 11 glycemic-controlled type 2 diabetic (T2D) individuals. We also assessed the dynamic change of mTORC1 activity in β cells of db/db mice with new-onset diabetes. Results There exists intercellular heterogeneity of mTORC1 activities in human islets. Islet mTORC1 activity was independently and positively correlated with FBG in ND, but not in IFG and T2D. Moreover, we did not detect significant change in mTORC1 activities between T2D and ND. Of note, the islet mTORC1 activities were significantly higher in IFG than in ND. We further stratified IFG individuals according to their islet PS6 levels and found that IFG-PS6high exhibited remarkably higher urocortin3 and glucose transporter 2 expression in their β cells compared to IFG-PS6low. Consistently, we also detected a significant increase in mTORC1 activities in prediabetic db/db mice compared to nondiabetic littermates. Interestingly, mTORC1 activities determined β-cell adaptation or failure in db/db mice: A strong negative correlation was found between islet mTORC1 activities and fasting glucose levels in db/db mice during their diabetes progression. Conclusions Our finding highlights a dynamic islet mTORC1 response in β-cell adaption/failure in human T2D.

scholarly journals Ishige okamurae reduces blood glucose levels in high-fat diet mice and improves glucose metabolism in the skeletal muscle and pancreas

2020 ◽  
Vol 23 (1) ◽  
Author(s):  
Hye-Won Yang ◽  
Myeongjoo Son ◽  
Junwon Choi ◽  
Seyeon Oh ◽  
You-Jin Jeon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Blood Glucose Level ◽  
High Fat Diet ◽  
Saline Group ◽  
High Fat ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Ishige Okamurae

Abstract Brown alga (Ishige okamurae; IO) dietary supplements have been reported to possess anti-diabetic properties. However, the effects of IO supplements have not been evaluated on glucose metabolism in the pancreas and skeletal muscle. C57BL/6 N male mice (age, 7 weeks) were arranged in five groups: a chow diet with 0.9% saline (NFD/saline group), high-fat diet (HFD) with 0.9% saline (HFD/saline group). high-fat diet with 25 mg/kg IO extract (HFD/25/IOE). high-fat diet with 50 mg/kg IO extract (HFD/50/IOE), and high-fat diet with 75 mg/kg IO extract (HFD/75/IOE). After 4 weeks, the plasma, pancreas, and skeletal muscle samples were collected for biochemical analyses. IOE significantly ameliorated glucose tolerance impairment and fasting and 2 h blood glucose level in HFD mice. IOE also stimulated the protein expressions of the glucose transporters (GLUTs) including GLUT2 and GLUT4 and those of their related transcription factors in the pancreases and skeletal muscles of HFD mice, enhanced glucose metabolism, and regulated blood glucose level. Our results suggest Ishige okamurae extract may reduce blood glucose levels by improving glucose metabolism in the pancreas and skeletal muscle in HFD-induced diabetes.

scholarly journals Antidiabetic Effect of Casein Glycomacropeptide Hydrolysates on High-Fat Diet and STZ-Induced Diabetic Mice via Regulating Insulin Signaling in Skeletal Muscle and Modulating Gut Microbiota

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 220 ◽  
Author(s):  
Qichen Yuan ◽  
Biyuan Zhan ◽  
Rui Chang ◽  
Min Du ◽  
Xueying Mao
Keyword(s):  
Skeletal Muscle ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Glycogen Synthase ◽  
Fasting Blood Glucose ◽  
Diabetic Mice ◽  
High Fat ◽  
Antidiabetic Effect ◽  
Glucose Levels

This study evaluated the effects and the underlying mechanisms of casein glycomacropeptide hydrolysate (GHP) on high-fat diet-fed and streptozotocin-induced type 2 diabetes (T2D) in C57BL/6J mice. Results showed that 8-week GHP supplementation significantly decreased fasting blood glucose levels, restored insulin production, improved glucose tolerance and insulin tolerance, and alleviated dyslipidemia in T2D mice. In addition, GHP supplementation reduced the concentration of lipopolysaccharides (LPSs) and pro-inflammatory cytokines in serum, which led to reduced systematic inflammation. Furthermore, GHP supplementation increased muscle glycogen content in diabetic mice, which was probably due to the regulation of glycogen synthase kinase 3 beta and glycogen synthase. GHP regulated the insulin receptor substrate-1/phosphatidylinositol 3-kinase/protein kinase B pathway in skeletal muscle, which promoted glucose transporter 4 (GLUT4) translocation. Moreover, GHP modulated the overall structure and diversity of gut microbiota in T2D mice. GHP increased the Bacteroidetes/Firmicutes ratio and the abundance of S24-7, Ruminiclostridium, Blautia and Allobaculum, which might contribute to its antidiabetic effect. Taken together, our findings demonstrate that the antidiabetic effect of GHP may be associated with the recovery of skeletal muscle insulin sensitivity and the regulation of gut microbiota.

scholarly journals Acute high-fat feeding leads to disruptions in glucose homeostasis and worsens stroke outcome

2017 ◽  
Vol 39 (6) ◽  
pp. 1026-1037 ◽  
Author(s):  
Michael J Haley ◽  
Siddharth Krishnan ◽  
David Burrows ◽  
Leon de Hoog ◽  
Jamie Thakrar ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Artery Occlusion ◽  
Experimental Stroke ◽  
High Fat ◽  
Glut 1 ◽  
Fat Consumption ◽  
Fat Feeding ◽  
The Brain

Chronic consumption of diets high in fat leads to obesity and can negatively affect brain function. Rodents made obese by long-term maintenance on a high-fat diet have worse outcome after experimental stroke. High-fat consumption for only three days does not induce obesity but has rapid effects on the brain including memory impairment. However, the effect of brief periods of high-fat feeding or high-fat consumption in the absence of obesity on stroke is unknown. We therefore tested the effect of an acute period of high-fat feeding (three days) in C57B/6 mice on outcome after middle cerebral artery occlusion (MCAo). In contrast to a chronic high-fat diet (7.5 months), an acute high-fat diet had no effect on body weight, adipose tissue, lipid profile or inflammatory markers (in periphery and the brain). Three days of high-fat feeding impaired glucose tolerance, increased plasma glucose and insulin and brain expression of the glucose transporter GLUT-1. Ischaemic damage was increased (48%) in mice fed an acute high-fat diet, and was associated with a further reduction in GLUT-1 in the ischaemic hemisphere. These data demonstrate that only a brief period of high-fat consumption has a negative effect on glucose homeostasis and worsens outcome after ischaemic stroke.

scholarly journals TGS1: a novel regulator of β-cell mass and function

2021 ◽  
Author(s):  
Manuel Blandino-Rosano ◽  
Pau Romaguera-Llacer ◽  
Ashley Lin ◽  
Janardan K Reddy ◽  
Ernesto Bernal-Mizrachi
Keyword(s):  
Cell Cycle ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Cell Function ◽  
Cell Mass ◽  
High Fat ◽  
Β Cells ◽  
Β Cell ◽  
Β Cell Function ◽  
And Function

Type 2 diabetes (T2D) is a metabolic disorder associated with abnormal glucose homeostasis and is characterized by intrinsic defects in β-cell function and mass. Trimethylguanosine synthase 1 (TGS1) is an evolutionarily conserved enzyme that methylates small nuclear and nucleolar RNAs (snRNAs and snoRNAs) and is involved in pre-mRNA splicing, transcription, and ribosome production. However, the role of TGS1 in β-cells and glucose homeostasis had not been explored. Here we show that TGS1 is upregulated by insulin and upregulated in islets from mice exposed to a high-fat diet and in human β-cells from T2D donors. Using mice with conditional (βTGS1KO and βTGS1Het) and inducible (MIP-CreERT-TGS1KO) TGS1 deletion, we determine that TGS1 regulates β-cell mass and function. Unbiased approaches allowed us to identify a link between TGS1 and ER stress and cell cycle arrest and how TGS1 regulates β-cell apoptosis. Deletion of TGS1 results in an increase in the unfolded protein response by increasing XBP-1, ATF-4, and the phosphorylation of eIF2α, and several changes in cell cycle inhibitors and activators such as p27 and Cyclin D2. This study establishes TGS1 as a key player regulating β-cell mass and function as well as playing a role in the adaptive β-cell function to a high-fat diet. These observations can be used as a stepping-stone for the design of novel strategies using TGS1 as a therapeutic target for the treatment of diabetes.

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