Theabrownin-targeted regulation of intestinal microorganisms to improve glucose and lipid metabolism in Goto-Kakizaki rats

Abstract Background: Abnormalities in lipid and glucose metabolism are are constantly occured in type 2 diabetes (T2DM). However, it can be ameliorated by gentiopicroside (GPS). Considering the key role of fibroblast growth factor receptor 1/phosphatidylinositol 3-kinase/protein kinase B (FGFR1/PI3K/AKT) pathway in T2DM, we explore the possible mechanism of GPS on lipid and glucose metabolism through its effects on FGFR1/PI3K/AKT pathway.Methods: Palmitic acid (PA)-induced HepG2 cells and a db/db mice were used to clarify the role and mechanism of polydatin on lipid and glucose metabolism.Results: GPS ameliorated glucose and lipid metabolism disorders in db/db mice and PA-induced HepG2 cells. Furthermore, GPS activated FGFR1/PI3K/AKT pathway including increased the protein expression of FGFR1 and promoted the phosphorylation of PI3K, AKT and FoxO1. Additionally, knockdown of FGFR1 reversed the activation of PI3K/AKT pathway by GPS.Conclusions: The present study demontrates that GPS ameliorates glucose and lipid metabolism disorders via activation of FGFR1/PI3K/AKT pathway.

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Differential hepatic gene expression in a polygenic mouse model with insulin resistance and hyperglycemia: evidence for a combined transcriptional dysregulation of gluconeogenesis and fatty acid synthesis

Journal of Molecular Endocrinology ◽

10.1677/jme.0.0320195 ◽

2004 ◽

Vol 32 (1) ◽

pp. 195-208 ◽

Cited By ~ 22

Author(s):

W Becker ◽

R Kluge ◽

T Kantner ◽

K Linnartz ◽

M Korn ◽

...

Keyword(s):

Gene Expression ◽

Insulin Resistance ◽

Fatty Acid ◽

Lipid Metabolism ◽

Glucose Metabolism ◽

Mrna Levels ◽

Insulin Resistant ◽

Glucose And Lipid Metabolism ◽

Nzo Mice ◽

Hepatic Glucose

New Zealand obese (NZO) mice exhibit severe insulin resistance of hepatic glucose metabolism. In order to define its biochemical basis, we studied the differential expression of genes involved in hepatic glucose and lipid metabolism by microarray analysis. NZOxF1 (SJLxNZO) backcross mice were generated in order to obtain populations with heterogeneous metabolism but comparable genetic background. In these backcross mice, groups of controls (normoglycemic/normoinsulinemic), insulin-resistant (normoglycemic/hyperinsulinemic) and diabetic (hyperglycemic/hypoinsulinemic) mice were identified. At 22 weeks, mRNA was isolated from liver, converted to cDNA, and used for screening of two types of cDNA arrays (high-density filter arrays and Affymetrix oligonucleotide microarrays). Differential gene expression was ascertained and assessed by Northern blotting. The data indicate that hyperinsulinemia in the NZO mouse is associated with: (i) increased mRNA levels of enzymes involved in lipid synthesis (fatty acid synthase, malic enzyme, stearoyl-CoA desaturase) or fatty acid oxidation (cytochrome P450 4A14, ketoacyl-CoA thiolase, acyl-CoA oxidase), (ii) induction of the key glycolytic enzyme pyruvate kinase, and (iii) increased mRNA levels of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. These effects were enhanced by a high-fat diet. In conclusion, the pattern of gene expression in insulin-resistant NZO mice appears to reflect a dissociation of the effects of insulin on genes involved in glucose and lipid metabolism. The data are consistent with a hypothetical scenario in which an insulin-resistant hepatic glucose production produces hyperinsulinemia, and an enhanced insulin- and substrate-driven lipogenesis further aggravates the deleterious insulin resistance of glucose metabolism.

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AMPK and Metabolisms of Glucose and Lipid

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.887-888.547 ◽

2014 ◽

Vol 887-888 ◽

pp. 547-550 ◽

Cited By ~ 1

Author(s):

Ying Chang ◽

Xin Jiang ◽

Yan Chun Wang

Keyword(s):

Lipid Metabolism ◽

Glucose Metabolism ◽

Glucose And Lipid Metabolism ◽

Structure Activity ◽

In Cells

AMPK is ubiquitous in eukaryotes.It takes part in cells metabolism and is called energy receptor.It is activated with AMP/ATP ratio increasing.At present,metformin is used to activate AMPK in order to regulate glucose metabolism and treat diabetes.In this article,we summarize the structure activity of AMPK and its effects on glucose and lipid metabolism.

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Muscle-specific TGR5 overexpression improves glucose clearance in glucose-intolerant mice

Journal of Biological Chemistry ◽

10.1074/jbc.ra120.016203 ◽

2020 ◽

pp. jbc.RA120.016203

Author(s):

Takashi Sasaki ◽

Yuichi Watanabe ◽

Ayane Kuboyama ◽

Akira Oikawa ◽

Makoto Shimizu ◽

...

Keyword(s):

Skeletal Muscle ◽

Lipid Metabolism ◽

Glucose Metabolism ◽

Glucose Utilization ◽

Glycolytic Flux ◽

Metabolism Disorder ◽

Glucose And Lipid Metabolism ◽

Physiological Processes ◽

Glucose Clearance ◽

Novel Strategy

TGR5, a G protein-coupled bile acid receptor, is expressed in various tissues and regulates several physiological processes. In the skeletal muscle, TGR5 activation is known to induce muscle hypertrophy; however, the effects on glucose and lipid metabolism are not well understood, despite the fact that the skeletal muscle plays a major role in energy metabolism. Here, we demonstrate that skeletal muscle-specific TGR5 transgenic (Tg) mice exhibit increased glucose utilization, without altering the expression of major genes related to glucose and lipid metabolism. Metabolite profiling analysis by CE-TOF MS showed that glycolytic flux was activated in the skeletal muscle of Tg mice, leading to an increase in glucose utilization. Upon long-term, high-fat diet (HFD) challenge, blood glucose clearance was improved in Tg mice without an accompanying increase in insulin sensitivity in skeletal muscle and a reduction of body weight. Moreover, Tg mice showed improved age-associated glucose intolerance. These results strongly suggest that TGR5 ameliorated glucose metabolism disorder that is caused by diet-induced obesity and aging by enhancing the glucose metabolic capacity of skeletal muscle. Our study demonstrates that TGR5 activation in the skeletal muscle is effective in improving glucose metabolism and may be beneficial in developing a novel strategy for the prevention or treatment of hyperglycemia.

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Maternal Gut Microbiota Transplantation Undermined the Lipid and Glucose Metabolism of Newborns in a Piglet Model

10.21203/rs.3.rs-104735/v1 ◽

2020 ◽

Author(s):

Hua Zhou ◽

Jing Sun ◽

Zuohua Liu ◽

Hong Chen ◽

Liangpeng Ge ◽

...

Keyword(s):

Lipid Metabolism ◽

Glucose Metabolism ◽

Gut Microbiota ◽

Fecal Microbiota Transplantation ◽

Fecal Microbiota ◽

Longissimus Dorsi ◽

Germ Free ◽

Newborn Piglets ◽

Glucose And Lipid Metabolism ◽

Fecal Suspension

Abstract BackgroundThe present study was conducted to explore the maternal gut microbiota transplantation on the lipid and glucose metabolism of newborns in a piglet model. Six hysterectomy-derived germ-free (GF) Bama piglets were reared in three sterile isolators and were orally inoculated with healthy sow fecal suspension on day 7 after birth, which considers as fecal microbiota transplanted (FMT) group. Another six piglets from a natural birth and reared in conventional (CV) environments was regarded as CV group. The FMT piglets were hand-fed Co60-γ-irradiated sterile milk powder, CV piglets were reared by lactating Bama sows and both were weaned at day 21. Then, all piglets were housed separately and fed sterile feed for another 21 days. ResultsWe observed that transplanted with sow fecal microbiota increased the content of lipid in liver (P < 0.05), and upregulated the mRNA abundances of genes related to lipid anabolism and catabolism in liver and longissimus dorsi of newborn piglets (P < 0.05). Meanwhile, the concentrations of adiponectin, GLP-1, and insulin in serum and the activity of CPT-1 in liver were lower in FMT piglets (P < 0.05). Besides, transplanted with sow fecal microbiota enhanced the concentration of glycogen in liver (P < 0.05), while upregulated the mRNA expressions of genes related to glycogenesis and glycogenolysis in liver and longissimus dorsi of newborn piglets (P < 0.05). Moreover, the pathway of AMPK was stimulated by sow fecal microbiota transplantation (P < 0.10). In addition, the microbial structure between FMT and CV piglets was marked differently (P < 0.05). Furthermore, transplanted with sow fecal microbiota markedly activated the metabolic pathway of bile secretion in newborn piglets (P < 0.05). ConclusionsCollectively, healthy sow gut microbiota transplanted to newborn germ-free piglets might undermine the homeostasis of glucose and lipid metabolism, and increased the content of lipid, and decreased the concentration of glycogen in liver. It is concluded that transplanted with maternal gut microbiota might induce diseases related to glucose and lipid metabolism in newborns.

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Glucose and Lipid Metabolism During Long-Term Treatment with Cilazapril in Hypertensive Patients With or Without Impaired Glucose Metabolism

Journal of Cardiovascular Pharmacology ◽

10.1097/00005344-199006000-00011 ◽

1990 ◽

Vol 15 (6) ◽

pp. 933-938 ◽

Cited By ~ 10

Author(s):

Hiroshi Shionoiri ◽

Koh-ichi Sugimoto ◽

Kohsuke Minamisawa ◽

Shin-ichiro Ueda ◽

Toshiaki Ebina ◽

...

Keyword(s):

Lipid Metabolism ◽

Glucose Metabolism ◽

Term Treatment ◽

Impaired Glucose Metabolism ◽

Hypertensive Patients ◽

Glucose And Lipid Metabolism ◽

Long Term Treatment

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Pioglitazone versus Rosiglitazone: Effects on Lipids, Lipoproteins, and Apolipoproteins in Head-to-Head Randomized Clinical Studies

PPAR Research ◽

10.1155/2008/520465 ◽

2008 ◽

Vol 2008 ◽

pp. 1-6 ◽

Cited By ~ 28

Author(s):

Mark A. Deeg ◽

Meng H. Tan

Keyword(s):

Clinical Trials ◽

Lipid Metabolism ◽

Glucose Metabolism ◽

Randomized Clinical Trials ◽

Peroxisome Proliferator ◽

Glucose Lowering ◽

Glucose And Lipid Metabolism ◽

Ppar Agonists ◽

Peroxisome Proliferator Activated Receptors ◽

Regulate Lipid Metabolism

Peroxisome proliferator-activated receptors (PPARs) play an important role in regulating both glucose and lipid metabolism. Agonists for both PPAR and PPAR have been used to treat dyslipidemia and hyperglycemia, respectively. In addition to affecting glucose metabolism, PPAR agonists also regulate lipid metabolism. In this review, we will focus on the randomized clinical trials that directly compared the lipid effects of the thiazolidinedione class of PPAR agonists, pioglitazone and rosiglitazone, head-to-head either as monotherapy or in combination with other lipid-altering or glucose-lowering agents

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