scholarly journals Maca extracts regulate glucose and lipid metabolism in insulin‐resistant HepG2 cells via the PI3K/AKT signalling pathway

2021 ◽  
Author(s):  
Aimin Li ◽  
Jia Liu ◽  
Fangli Ding ◽  
Xiaolei Wu ◽  
Cong Pan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Signalling Pathway ◽  
Insulin Resistant ◽  
Glucose And Lipid Metabolism

Effects of VO2 nanoparticles on human liver HepG2 cells: Cytotoxicity, genotoxicity, and glucose and lipid metabolism disorders

NanoImpact ◽  
2021 ◽  
Vol 24 ◽  
pp. 100351
Author(s):  
Jia-Bei Li ◽  
Wen-Song Xi ◽  
Shi-Ying Tan ◽  
Yuan-Yuan Liu ◽  
Hao Wu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

Improvement of glucose and lipid metabolism in diabetic rats treated with molybdate

1996 ◽  
Vol 270 (2) ◽  
pp. E344-E352 ◽  
Author(s):  
A. T. Ozcelikay ◽  
D. J. Becker ◽  
L. N. Ongemba ◽  
A. M. Pottier ◽  
J. C. Henquin ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Synthase ◽  
Diabetic Rats ◽  
Nonesterified Fatty Acids ◽  
Insulin Resistant ◽  
Hepatic Glucose Metabolism ◽  
Glucose And Lipid Metabolism ◽  
Glycogen Stores

Molybdenum mimics certain insulin actions in vitro. We have investigated the effects of oral administration of Na2MoO4 (Mo) for 8 wk on carbohydrate and lipid metabolism in streptozotocin-diabetic rats. Mo decreased hyperglycemia and glucosuria by 75% and corrected the elevation of plasma nonesterified fatty acids. Tolerance to glucose loads was improved, and glycogen stores were replenished. These effects were not due to a rise of insulinemia. In liver, Mo restored the blunted mRNA and activity of glucokinase and pyruvate kinase and decreased to normal phosphoenolpyruvate carboxykinase values. Finally, Mo totally reversed the low expression and activity of acetyl-CoA carboxylase and fatty acid synthase in liver, but not in white adipose tissue. In conclusion, Mo exerts a marked blood glucose-lowering effect in diabetic rats by an insulin-like action. This effect results in part from a restoration of hepatic glucose metabolism and is associated with a tissue-specific correction of lipogenic enzyme gene expression, both processes being essentially mediated by reversal of impaired pretranslational regulatory mechanisms. These observations raise new therapeutic perspectives in diabetes, particularly in the insulin-resistant condition.

scholarly journals Possible interactions between angiotensin II and insulin: effects on glucose and lipid metabolism in vivo and in vitro

2000 ◽  
Vol 167 (3) ◽  
pp. 525-531 ◽  
Author(s):  
D Patiag ◽  
X Qu ◽  
S Gray ◽  
I Idris ◽  
M Wilkes ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Insulin Resistant ◽  
Receptor Mrna ◽  
Glucose And Lipid Metabolism ◽  
Sd Rats ◽  
Insulin Antagonist ◽  
Antagonist Effect

Angiotensin II (ANGII) increases insulin sensitivity in diabetic and non-diabetic subjects, even at subpressor doses, and because there is 'crosstalk' between ANGII and insulin-signaling pathways the underlying mechanism may not be due solely to changes in regional blood flow. A series of experimental studies was undertaken to evaluate the effects of ANGII on glucose and lipid metabolism in vivo and in vitro. Groups of fructose-fed, insulin-resistant Sprague-Dawley (SD) rats were pre-treated with 0.3 mg/kg per day of the AT(1)-receptor antagonist L-158 809 (n=16), or vehicle (n=16), by oral gavage. This was prior to an oral glucose tolerance test (day 5) and measurement of the effects of ANGII infusion (20 ng/kg per min i.v. for 3 h) on whole-body insulin sensitivity using the insulin suppression test (day 7). The effect of ANGII infusion on total triglyceride secretion rate (TGSR) was evaluated in normal SD rats pretreated for 7 days with L-158 809 (n=12) or vehicle (n=12). AT(1)- and AT(2)- receptor mRNA expression and [(3)H]2-deoxyglucose uptake were assessed in cultured L6 myoblasts. Short-term treatment with L-158 809 had no effect on glucose tolerance or fasting triglyceride levels in fructose-fed rats. ANGII infusion had no effect on insulin sensitivity in fructose-fed rats pretreated with vehicle (steady-state plasma glucose (SSPG) values 8.1+/-1.6 vs 8. 4+/-0.4 mmol/l), but pretreatment with L-158 809 resulted in ANGII having a modest insulin antagonist effect in this insulin-resistant model (SSPG values 9.6+/-0.3 vs 7.1+/-0.6, P<0.03). ANGII infusion had no significant effect on TGSR (e.g. 24.6+/-1.4 vs 28.4+/-0.9 mg/100 g per h in vehicle-treated animals). RT-PCR analysis showed that L6 cells express both AT(1)- and AT(2)-receptor mRNA. Incubation with ANGII (10(-9) and 10(-8) M) had no significant effect on the dose-response curve for insulin-stimulated [(3)H]2-deoxyglucose uptake. For example, C(I200) values (dose of insulin required to increase glucose uptake by 200%) were 4.5 x 10(-9) M (control) vs 3.9 x 10(-9) M and 6.2 x 10(-9) M, whereas the positive control (glucagon-like peptide-1) increased insulin sensitivity. Thus, ANGII infusion may have a modest insulin antagonist effect on glucose disposal in insulin-resistant fructose-fed rats pretreated with an AT(1)-blocker, but ANGII has no effect on TGSR or in vitro glucose uptake in L6 myoblasts. These findings are relevant to recent clinical discussions about the metabolic effects of ANGII and renin-angiotensin system blockade.

scholarly journals The Aqueous Extract of Gynura divaricata (L.) DC. Improves Glucose and Lipid Metabolism and Ameliorates Type 2 Diabetes Mellitus

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Jinnan Li ◽  
Jinlei Feng ◽  
Hong Wei ◽  
Qunying Liu ◽  
Ting Yang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Water Extract ◽  
The Body ◽  
Peripheral Tissues ◽  
Insulin Resistant ◽  
Glucose And Lipid Metabolism

Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by hyperglycemia and dyslipidemia caused by impaired insulin secretion and resistance of the peripheral tissues. A major pathogenesis of T2DM is obesity-associated insulin resistance. Gynura divaricata (L.) DC. (GD) is a natural plant and has been reported to have numerous health-promoting effects on both animals and humans. In this study, we aimed to elucidate the regulatory mechanism of GD improving glucose and lipid metabolism in an obesity animal model induced by high-fat and high-sugar diet in combination with low dose of streptozocin and an insulin-resistant HepG2 cell model induced by dexamethasone. The study showed that the water extract of GD (GD extract A) could significantly reduce fasting serum glucose, reverse dyslipidemia and pancreatic damage, and regulate the body weight of mice. We also found that GD extract A had low toxicity in vivo and in vitro. Furthermore, GD extract A may increase glucose consumption in insulin-resistant HepG2 cells, markedly inhibit NF-κB activation, and decrease the impairment in signaling molecules of insulin pathway, such as IRS-1, AKT, and GLUT1. Overall, the results indicate that GD extract A is a promising candidate for the prevention and treatment of T2DM.

Sensing Nuclear Glucose

2007 ◽  
Vol 2007 (369) ◽  
pp. tw20-tw20
Author(s):  
Elizabeth M. Adler
Keyword(s):  
Lipid Metabolism ◽  
Transcriptional Activation ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Glucose Sensor ◽  
Acid Synthesis ◽  
Cholesterol Homeostasis ◽  
Binding Domains ◽  
Glucose And Lipid Metabolism ◽  
X Receptors

The liver X receptors (LXR-α and -β) are nuclear transcription factors that have been implicated in both glucose and lipid metabolism; their activation by oxysterol ligands elicits both a decrease in atherosclerosis and antidiabetic effects. Although synthetic LXR ligands decrease hepatic gluconeogenesis and increase lipogenesis in rodent models, the normal rodent diet lacks cholesterol, which led Mitro et al. to search for other ligands. They found that glucose and glucose derivatives stimulated the transcriptional activation of a Gal4-responsive gene reporter in human HepG2 cells expressing constructs in which LXR ligand-binding domains (LBDs) were fused to the Gal4 DNA binding domain and transcriptionally activated LXR-RXR (retinoid X receptor) targets. Cell-free coactivator recruitment assays and scintillation proximity assays indicated that glucose and glucose-6-phosphate were direct LXR agonists that bound to the LXR LBD. Furthermore, glucose protected LXR-α from proteolytic attack and increased the LXR-β melting temperature. Glucose had effects on the transcription of LXR target genes in HEPG2 cells similar to those of known ligands, stimulating the expression of genes involved in fatty acid synthesis and cholesterol homeostasis and inhibiting expression of gluconeogenic genes; moreover, it potentiated the effects of LXR ligands. Similarly, glucose- or sucrose-feeding stimulated the expression of LXR target genes in the livers of fasted mice, even mice that were insulin deficient. Thus, glucose itself appears to act as a ligand for LXR, leading the authors to propose that LXR acts as a "transcriptional switch" to coordinate carbohydrate and lipid metabolism. N. Mitro, P. A. Mak, L. Vargas, C. Godio, E. Hampton, V. Molteni, A. Kreusch, E. Saez, The nuclear receptor LXR is a glucose sensor. Nature445, 219-223 (2007). [PubMed]

scholarly journals Glucose Tolerance-Improving Activity of Helichrysoside in Mice and Its Structural Requirements for Promoting Glucose and Lipid Metabolism

2019 ◽  
Vol 20 (24) ◽  
pp. 6322
Author(s):  
Morikawa ◽  
Nagatomo ◽  
Oka ◽  
Miki ◽  
Taira ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Organic Acids ◽  
Hepg2 Cells ◽  
Glucose Consumption ◽  
Liver Weight ◽  
Flavonol Glycosides ◽  
Plasma Parameters ◽  
Structural Requirements ◽  
Glucose And Lipid Metabolism

An acylated flavonol glycoside, helichrysoside, at a dose of 10 mg/kg/day per os for 14 days, improved the glucose tolerance in mice without affecting the food intake, visceral fat weight, liver weight, and other plasma parameters. In this study, using hepatoblastoma-derived HepG2 cells, helichrysoside, trans-tiliroside, and kaempferol 3-O-β-D-glucopyranoside enhanced glucose consumption from the medium, but their aglycones and p-coumaric acid did not show this activity. In addition, several acylated flavonol glycosides were synthesized to clarify the structural requirements for lipid metabolism using HepG2 cells. The results showed that helichrysoside and related analogs significantly inhibited triglyceride (TG) accumulation in these cells. The inhibition by helichrysoside was more potent than that by other acylated flavonol glycosides, related flavonol glycosides, and organic acids. As for the TG metabolism-promoting activity in high glucose-pretreated HepG2 cells, helichrysoside, related analogs, and their aglycones were found to significantly reduce the TG contents in HepG2 cells. However, the desacyl flavonol glycosides and organic acids derived from the acyl groups did not exhibit an inhibitory impact on the TG contents in HepG2 cells. These results suggest that the existence of the acyl moiety at the 6'' position in the D-glucopyranosyl part is essential for glucose and lipid metabolism-promoting activities.

scholarly journals Green Tea Polyphenol Epigallocatechin-3-Gallate Enhance Glycogen Synthesis and Inhibit Lipogenesis in Hepatocytes

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Jane J. Y. Kim ◽  
Yi Tan ◽  
Linda Xiao ◽  
Ya-Li Sun ◽  
Xianqin Qu
Keyword(s):  
Lipid Metabolism ◽  
Green Tea ◽  
Hepg2 Cells ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Green Tea Polyphenols ◽  
Dependent Manner ◽  
Beneficial Effects ◽  
Glucose And Lipid Metabolism ◽  
Green Tea Polyphenol

The beneficial effects of green tea polyphenols (GTP) against metabolic syndrome and type 2 diabetes by suppressing appetite and nutrient absorption have been well reported. However the direct effects and mechanisms of GTP on glucose and lipid metabolism remain to be elucidated. Since the liver is an important organ involved in glucose and lipid metabolism, we examined the effects and mechanisms of GTP on glycogen synthesis and lipogenesis in HepG2 cells. Concentrations of GTP containing 68% naturally occurring (−)-epigallocatechin-3-gallate (EGCG) were incubated in HepG2 cells with high glucose (30 mM) under 100 nM of insulin stimulation for 24 h. GTP enhanced glycogen synthesis in a dose-dependent manner. 10 μM of EGCG significantly increased glycogen synthesis by 2fold (P<0.05) compared with insulin alone. Western blotting revealed that phosphorylation of Ser9 glycogen synthase kinase 3βand Ser641 glycogen synthase was significantly increased in GTP-treated HepG2 cells compared with nontreated cells. 10 μM of EGCG also significantly inhibited lipogenesis (P<0.01). We further demonstrated that this mechanism involves enhanced expression of phosphorylated AMP-activated protein kinaseαand acetyl-CoA carboxylase in HepG2 cells. Our results showed that GTP is capable of enhancing insulin-mediated glucose and lipid metabolism by regulating enzymes involved in glycogen synthesis and lipogenesis.

Sign in / Sign up

Export Citation Format

Share Document