The Effect of FGF-21 on Glucose Metabolism in The Resistin-induced Insulin Resistance Liver Cells

2013 ◽  
Vol 40 (6) ◽  
pp. 524
Author(s):  
Miao LIU ◽  
Wen-Fei WANG ◽  
Ming-Yao LIU ◽  
Jing-Zhuang ZHAO ◽  
Yin BAI ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Liver Cells

In Vitro Diabetogenic Effect of Cadmium on Liver

2017 ◽  
Vol 8 (01) ◽  
Author(s):  
Agung Biworo ◽  
Dwi Rezki Amalia ◽  
Gratianus Billy Himawan ◽  
Lisda Rizky Amalia ◽  
Valentina Halim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Liver Homogenate ◽  
Liver Cells ◽  
Male Rats ◽  
Glycogen Level ◽  
Liver Sample ◽  
Km Value ◽  
Cd Exposure ◽  
Menten Constant

The objectives of this study were to determine the effect of cadmium (Cd) on glucose metabolism disruption in liver cells homogenate in vitro. The glucose metabolism disruption was analyzed by measuring the level of liver glucose, glycogen and methylglyoxal (MG), and the activity of glucokinase activity. In this experiment, a liver sample was taken from male rats (Rattus novergicus). Samples then homogenized and divided into four groups with; C served as control which contains liver homogenate only; T1 which contains liver homogenate + 0.03 mg/l of cadmium sulphate (CdSO4); T2 which contains liver homogenate + 0.3 mg/l of CdSO4; and T3 which contains liver homogenate + 3 mg/l of CdSO4. After treatment, liver glucose, glycogen, and MG levels, and glucokinase activity were estimated. The activity of liver glucokinase was estimated by measuring the Michaelis-Menten constant (Km) value. The results revealed that Cd exposure could significantly increase glucose and MG levels, the Km value of glucokinase, and decreased the glycogen level in liver cells (P>0.05). These results indicated that Cd exposure induced the disruption of glucose metabolism in the liver.

The Protective Efficacy of Ethanolic Leaves Extract of Citronella Gras (Cymbopogon nardus) on Glucose Metabolism Alteration Induced By Mercury in Rats

2017 ◽  
Vol 9 (03) ◽  
Author(s):  
Fransisca Diana Alexandra ◽  
Dian Mutiasari ◽  
Trilianty Lestarisa ◽  
Eko Suhartono
Keyword(s):  
Glucose Metabolism ◽  
Protective Effect ◽  
Plant Extract ◽  
Protective Efficacy ◽  
Liver Weight ◽  
Liver Glycogen ◽  
Liver Cells ◽  
Glycogen Level ◽  
Group I ◽  
Citronella Grass

The present study was undertaken to investigate the protective effect of ethanolic citronella grass (C. nardus) leaves extract against mercury (Hg) induced glucose metabolism alteration in rats. Four groups of rats were selected, with 6 rats for each group. Animals of group I was received a 1 ppm of Hg only. Animals of groups II, III, and IV received a combination of 1 ppm Hg and plant extract in different dose (1650, 2520, and 3360 mg/ml). The experiment lasted for 4 weeks. The various parameters studied included liver weight, liver glucose, glycogen, and malondialdehyde (MDA) level in all groups after treatment. The results of this present studies showed that the Hg-induced glucose metabolism alteration in rats which can be seen from the increase of liver glucose and the decreasing of liver glycogen levels. The results also showed that the Hginduced glucose metabolism alteration through its activities in the trigger the liver cells damage which can be seen from the decreasing of liver weight and the increase of liver MDA level. The ethanolic of C. nardus leaves extract shows a protective effect to maintain all parameters into a better a condition which can be seen from the significant increase in liver weight and liver glycogen level, and the significant decrease in liver glucose and MDA levels. The present study indicated that the ethanolic C. nardus leaves extract showed a potential protective effect on glucose metabolism alteration induced by Hg

Mass Spectrometry-based Label-free Quantitative Proteomic Analysis of CCl4-induced Acute Liver Injury in Mice Intervened by Total Glycosides from Ligustri Lucidi Fructus

2020 ◽  
Vol 17 ◽  
Author(s):  
Qian Lu ◽  
Hai-Zhu Xing ◽  
Nian-Yun Yang
Keyword(s):  
Insulin Resistance ◽  
Liver Injury ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Proteomic Analysis ◽  
Acute Liver Injury ◽  
Liver Cells ◽  
Differentially Expressed ◽  
Liver Protein ◽  
Differentially Expressed Proteins

Background: CCl4 acute liver injury (ALI) is a classical model for experimental research. However, there are few reports involved in the fundamental research of CCl4-induced ALI Ligustri Lucidi Fructus (LLF) are and its prescription have been used to treat hepatitis illness clinically. LLF and its active ingredients displayed anti-hepatitis effects, but the mechanism of function has not been fully clarified Objective: To investigate the proteomic analysis of CCl4-induced ALI, and examine the effects of active total glycosides (TG) from LLF on ALI of mice4, including histopathological survey and proteomic changes of liver tissues, and delineate the possible underlying mechanism. Methods: CCl4 was used to produce ALI mice model. The model mice were intragastrically administrated with TG and the liver his-topathological changes of mice were examined. At the end of test, mice liver samples were collected, after protein denaturation, re-duction, desalination and enzymatic hydrolysis, identification was carried out by nano LC-ESI-OrbiTrap MS/MS technology. The data was processed by Maxquant software. The differentially-expressed proteins were screened and identified, and their biological information was also analyzed based on GO and KEGG analysis. Key protein expression was validated by Western blot analysis Results: A total of 705 differentially-expressed proteins were identified during the normal, model and administration group. 9 signifi-cant differential proteins were focused based on analysis. Liver protein expression changes of CCl4-induced ALI mice were mainly involved in several important signal channels, namely FoxO signaling pathway, autophagy-animal, insulin signaling pathway. TG has anti-liver damnification effect in ALI mice, the mechanism of which is related to FoxO1 and autophagy pathways Conclusion: CCl4 inhibited expression of insulin-Like growth factor 1 (Igf1) and 3-phosphoinositide-dependent protein kinase 1 (Pdpk1) in liver cells and induced insulin resistance, thus interfered with mitochondrial autophagy and regeneration of liver cells and the metabolism of glucose and lipid, and caused hepatic necrosis in mice. TG resisted liver injury in mice. TG adjusted the expression level of key proteins Igf1 and Pdpk1 after liver injury and improved insulin resistance, thus promoted autophagy and resisted the liver damage

scholarly journals Brain Glucose Metabolism in Health, Obesity, and Cognitive Decline—Does Insulin Have Anything to Do with It? A Narrative Review

2021 ◽  
Vol 10 (7) ◽  
pp. 1532
Author(s):  
Eleni Rebelos ◽  
Juha O. Rinne ◽  
Pirjo Nuutila ◽  
Laura L. Ekblad
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Cognitive Decline ◽  
Fdg Pet ◽  
Metabolic Disorders ◽  
Brain Glucose ◽  
Brain Glucose Metabolism ◽  
Systemic Insulin Resistance ◽  
Increased Risk ◽  
18F Fdg

Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fasting [18F]-FDG-PET changes that occur in AD, recent evidence has shown alterations in fasting and insulin-stimulated brain glucose metabolism also in obesity and systemic insulin resistance. Thus, it is important to clarify whether changes in brain glucose metabolism are just an epiphenomenon of the pathophysiology of the metabolic and neurologic disorders, or a crucial determinant of their pathophysiologic cascade. In this review, we discuss the current knowledge regarding alterations in brain glucose metabolism, studied with [18F]-FDG-PET from metabolic disorders to AD, with a special focus on how manipulation of insulin levels affects brain glucose metabolism in health and in systemic insulin resistance. A better understanding of alterations in brain glucose metabolism in health, obesity, and neurodegeneration, and the relationships between insulin resistance and central nervous system glucose metabolism may be an important step for the battle against metabolic and cognitive disorders.

Impact of Glucose Metabolism Disorders on IGF-1 Levels in Patients with Acromegaly

2018 ◽  
Vol 50 (05) ◽  
pp. 408-413 ◽  
Author(s):  
Sema Dogansen ◽  
Gulsah Yalin ◽  
Seher Tanrikulu ◽  
Sema Yarman
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Glucose Metabolism Disorders ◽  
Insulin Resistant ◽  
Normal Glucose ◽  
Resistant Group ◽  
The Impact

AbstractIn this study, we aimed to evaluate the presence of glucose metabolism abnormalities and their impact on IGF-1 levels in patients with acromegaly. Ninety-three patients with acromegaly (n=93; 52 males/41 females) were included in this study. Patients were separated into three groups such as; normal glucose tolerance (n=23, 25%), prediabetes (n=38, 41%), and diabetes mellitus (n=32, 34%). Insulin resistance was calculated with homeostasis model assessment (HOMA). HOMA-IR > 2.5 or ≤2.5 were defined as insulin resistant or noninsulin resistant groups, respectively. Groups were compared in terms of factors that may be associated with glucose metabolism abnormalities. IGF-1% ULN (upper limit of normal)/GH ratios were used to evaluate the impact of glucose metabolism abnormalities on IGF-1 levels. Patients with diabetes mellitus were significantly older with an increased frequency of hypertension (p<0.001, p=0.01, respectively). IGF-1% ULN/GH ratio was significantly lower in prediabetes group than in normal glucose tolerance group (p=0.04). Similarly IGF-1% ULN/GH ratio was significantly lower in insulin resistant group than in noninsulin resistant group (p=0.04). Baseline and suppressed GH levels were significantly higher in insulin resistant group than in noninsulin resistant group (p=0.024, p<0.001, respectively). IGF-1% ULN/GH ratio is a useful marker indicating glucose metabolism disorders and IGF-1 levels might be inappropriately lower in acromegalic patients with insulin resistance or prediabetes. We suggest that IGF-1 levels should be re-evaluated after the improvement of insulin resistance or glycemic regulation for the successful management of patients with acromegaly.

scholarly journals Beneficial Effect of Pistachio Consumption on Glucose Metabolism, Insulin Resistance, Inflammation, and Related Metabolic Risk Markers: A Randomized Clinical Trial

Diabetes Care ◽  
2014 ◽  
Vol 37 (11) ◽  
pp. 3098-3105 ◽  
Author(s):  
Pablo Hernández-Alonso ◽  
Jordi Salas-Salvadó ◽  
Mònica Baldrich-Mora ◽  
Martí Juanola-Falgarona ◽  
Mònica Bulló
Keyword(s):  
Insulin Resistance ◽  
Clinical Trial ◽  
Glucose Metabolism ◽  
Beneficial Effect ◽  
Randomized Clinical Trial ◽  
Metabolic Risk ◽  
Risk Markers

scholarly journals Impact of disease activity on impaired glucose metabolism in patients with rheumatoid arthritis

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Gorica G. Ristić ◽  
Vesna Subota ◽  
Dejana Stanisavljević ◽  
Danilo Vojvodić ◽  
Arsen D. Ristić ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Disease Activity ◽  
Impaired Glucose Metabolism ◽  
Inflammation Markers ◽  
C Peptide ◽  
Related Risk ◽  
The Impact

Abstract Objective To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3). Methods This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses. Results RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient’s global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R2), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2–2.5) vs. 1.2 (0.8–1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9–1.9) vs. 1.2 (0.8–1.4), P = 0.375]. Conclusions RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.

Association between sleep disordered breathing in early pregnancy and glucose metabolism

SLEEP ◽  
2022 ◽  
Author(s):  
Laura Sanapo ◽  
Margaret H Bublitz ◽  
Alice Bai ◽  
Niharika Mehta ◽  
Geralyn M Messerlian ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Glucose Metabolism ◽  
Early Pregnancy ◽  
Airway Pressure ◽  
Sleep Disordered Breathing ◽  
Positive Airway Pressure ◽  
Obstructive Sleep ◽  
Respiratory Event

Abstract Study Objectives To examine the association between maternal sleep disordered breathing (SDB) and glucose metabolism in early gestation. Methods Women with body mass index (BMI) ≥27 kg/m2 and singleton pregnancies underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) in early pregnancy. Insulin resistance (HOMA-IR) and β-cell function (HOMA %B) were derived. Exclusion criteria included pregestational diabetes, use of continuous positive airway pressure and chronic steroid therapy. We performed linear regression analyses to evaluate the association between continuous measures of SDB (respiratory event index (REI), and oxygen desaturation index (ODI)) and glucose metabolism parameters (HOMA-IR and HOMA %B). Analyses were adjusted for a set of a priori selected variables which included gestational age, maternal age, BMI, ethnicity, race, and parity. Results One hundred and ninety-two pregnant women with median (interquartile range) BMI of 35.14 (8.30) kg/m2 underwent HSAT and HOMA assessment at 11.14 (3) and 15.35 (4.14) gestational weeks, respectively. REI and ODI, as continuous values, were associated with HOMA-IR after adjusting for covariates. OSA (obstructive sleep apnea) diagnosis (REI &gt; 5 events per hour) was not associated with HOMA-IR after adjusting for BMI (p ≥ 0.05). None of the parameters were associated with HOMA %B (p &gt; 0.07). Conclusions SDB and insulin resistance are associated in early pregnancy, with a dose response association between respiratory event index severity and insulin resistance. Further studies are needed to establish if pregnant women with overweight and obesity may benefit from early SDB screening to improve glucose metabolic outcome. Clinical trials: NCT02412696, Positive Airway Pressure, Sleep Apnea, and the Placenta (PAP-SAP) https://clinicaltrials.gov/ct2/show/NCT02412696?term=Bourjeily&draw=2&rank=2 and NCT02917876, Predictors of De-novo Development of Obstructive Sleep Apnea in Pregnancy (Predictors) https://clinicaltrials.gov/ct2/show/NCT02917876?term=Bourjeily&draw=2&rank=1

Berberine and Ginsenoside Rb1 Ameliorate Depression-Like Behavior in Diabetic Rats

2021 ◽  
pp. 1-19
Author(s):  
Jing-Hua Zhang ◽  
Hui-Zeng Yang ◽  
Hao Su ◽  
Jun Song ◽  
Yu Bai ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Morphological Changes ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Mild Stress ◽  
Ginsenoside Rb1 ◽  
Nissl Staining

Rhizoma coptidis(Huang-lian) and Asian ginseng have been widely used in the treatment of diabetes and other concurrent diseases with apparent effects. This study investigated the effects of the active ingredients of R. coptidis and ginseng, berberine and ginsenoside Rb1, on depression-like behavior in a rat diabetes model. The animal model was established via a high-fat diet and intraperitoneal injection of streptozotocin, while the animal’s depression-like behavior was induced via chronic unpredictable mild stress. These experimental rats were divided into four groups: control, depression-like behavior (DLB), metformin plus fluoxetine hydrochloride (M+FH), and berberine plus ginsenoside Rb1 (B+GRb1) groups. Glucose metabolism and insulin resistance were evaluated by oral glucose test and glucose clamp study. Depression-like behavior was evaluated via behavioral analyses, including forced swim, sucrose preference, elevated plus maze, and open-field tests. HE and Nissl staining, plasma cortisol expression of adrenocorticotropic hormone, and brain-derived neurotrophic factor (BDNF) levels were assayed to explore the mechanisms of action. Compared with the control, rats in the DLB group had a significant increase in the levels of blood glucose and depression-like behavior. The B+GRb1 group significantly improved glucose metabolism and insulin resistance, reduced depression-like behavior, downregulated levels of plasma cortisol and adrenocorticotropic hormone under stress, and upregulated BDNF protein expression compared to the DLB rats. HE and Nissl staining data revealed that B+GRb1 protected neurons from pathological and morphological changes. Thus, berberine and ginsenoside Rb1 not only improved glucose metabolism in diabetic rats but also ameliorated their depression-like behavior under chronic unpredictable stress. Mechanistically, studied data with plasma hormonal levels and brain neuronal pathological/morphological changes supported the observed effects. The combination of berberine and ginsenoside Rb1 may have a clinical value in the management of diabetic patients with depression.

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