scholarly journals Interplay Between Insulin Resistance and Body Fat Mass in Evolution of Perturbations Linked to the Metabolic Syndrome in Non-Diabetics: Emphasis on Inflammatory Factors

2020 ◽  
pp. 1-10
Author(s):  
Harry G. Preuss ◽  
Gilbert R. Kaats ◽  
Nate Mrvichin ◽  
Okezie I. Aruoma ◽  
Debasis Bagchi
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Fat ◽  
Fat Mass ◽  
Inflammatory Factors ◽  
Body Fat Mass ◽  
The Metabolic Syndrome

scholarly journals Dietary Isoliquiritigenin at a Low Dose Ameliorates Insulin Resistance and NAFLD in Diet-Induced Obesity in C57BL/6J Mice

2018 ◽  
Vol 19 (10) ◽  
pp. 3281 ◽  
Author(s):  
Youngmi Lee ◽  
Eun-Young Kwon ◽  
Myung-Sook Choi
Keyword(s):  
Insulin Resistance ◽  
Energy Expenditure ◽  
Body Fat ◽  
Fat Mass ◽  
High Fat Diet ◽  
Plasma Cholesterol ◽  
Cellular Respiration ◽  
Body Fat Mass ◽  
High Fat ◽  
Diet Induced Obesity

Isoliquiritigenin (ILG) is a flavonoid constituent of Glycyrrhizae plants. The current study investigated the effects of ILG on diet-induced obesity and metabolic diseases. C57BL/6J mice were fed a normal diet (AIN-76 purified diet), high-fat diet (40 kcal% fat), and high-fat diet +0.02% (w/w) ILG for 16 weeks. Supplementation of ILG resulted in decreased body fat mass and plasma cholesterol level. ILG ameliorated hepatic steatosis by suppressing the expression of hepatic lipogenesis genes and hepatic triglyceride and fatty acid contents, while enhancing β-oxidation in the liver. ILG improved insulin resistance by lowering plasma glucose and insulin levels. This was also demonstrated by the intraperitoneal glucose tolerance test (IPGTT). Additionally, ILG upregulated the expression of insulin signaling-related genes in the liver and muscle. Interestingly, ILG elevated energy expenditure by increasing the expression of thermogenesis genes, which is linked to stimulated mitochondrial biogenesis and uncoupled cellular respiration in brown adipose tissue. ILG also suppressed proinflammatory cytokine levels in the plasma. These results suggest that ILG supplemented at 0.02% in the diet can ameliorate body fat mass, plasma cholesterol, non-alcoholic fatty liver disease, and insulin resistance; these effects were partly mediated by increasing energy expenditure in high-fat fed mice.

scholarly journals Decreased Plasma Adiponectin Concentrations in Women with Dyslipidemia

2002 ◽  
Vol 87 (6) ◽  
pp. 2764-2769 ◽  
Author(s):  
Miyao Matsubara ◽  
Shoji Maruoka ◽  
Shinji Katayose
Keyword(s):  
Total Cholesterol ◽  
Body Fat ◽  
Fat Mass ◽  
Atherogenic Index ◽  
Body Fat Mass ◽  
Apo B ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Apo E ◽  
Wide Range

Adiponectin, the gene product of the adipose most abundant gene transcript 1, is a novel adipocyte-derived peptide that has been considered to have antiinflammatory and antiatherogenic effects. To characterize the relationship between adiponectin and lipids metabolism, we measured fasting plasma adiponectin concentration by ELISA, serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and apolipoprotein (apo) levels in 352 nondiabetic women, 16–86 yr old, with a wide range of body weight [body mass index (BMI), 14.8−36.3 kg/m2]. Plasma adiponectin concentrations in women with the highest tertile of TG (1.69 mm ≤ ∼) were decreased, compared with the middle (1.13 ≤ ∼ <1.69) or lowest tertile of TG (∼ <1.13) (5.9 ± 0.5 vs. 7.5 ± 0.3, 9.2 ± 0.2 μg/ml; P < 0.005, 0.001). Plasma adiponectin with the lowest tertile of HDL-C (∼ <1.16 mm) was decreased, compared with the middle (1.16 ≤ ∼ < 1.81) or highest tertile of HDL-C (1.81 ≤ ∼) (5.7 ± 0.5 vs. 7.8 ± 0.2, 10.1 ± 0.4 μg/ml; both P < 0.001). These relationships had similar tendencies after adjustment for BMI, body fat mass, age, or diastolic blood pressure. Adiponectin was negatively correlated with serum TG (r = −0.33, P < 0.0001), atherogenic index [(total cholesterol − HDL-C)/HDL-C] (r = −0.34, P < 0.0001), apo B (r = −0.45, P < 0.0001), or apo E (r = −0.29, P < 0.05), and positively correlated with serum HDL-C (r = 0.39, P < 0.0001) or apo A-I levels (r = 0.42, P < 0.002). Those negative relationships became stronger after adjusting for BMI or body fat mass. The slightly positive correlation between adiponectin and age, blood urea nitrogen, or creatinine levels was also observed (all P < 0.001). These results indicate that high-TGnemia and low-HDL-Cnemia are associated with low plasma adiponectin concentrations in nondiabetic women. Further efforts must now be targeted to determine whether adiponectin causes these lipid abnormalities and thus whether it is partly responsible for the atherogenic risk seen in the metabolic syndrome.

scholarly journals Body fat mass and the proportion of very large adipocytes in pregnant women are associated with gestational insulin resistance

2015 ◽  
Vol 40 (4) ◽  
pp. 646-653 ◽  
Author(s):  
H Svensson ◽  
L Wetterling ◽  
M Bosaeus ◽  
B Odén ◽  
A Odén ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Pregnant Women ◽  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass

scholarly journals Dihydromyricetin Ameliorates Inflammation-Induced Insulin Resistance via Phospholipase C-CaMKK-AMPK Signal Pathway

2021 ◽  
Author(s):  
Lianjie Hou ◽  
Fangyi Jiang ◽  
Bo Huang ◽  
Weijie Zheng ◽  
Yufei Jiang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Phospholipase C ◽  
Therapeutic Strategy ◽  
Public Health Problem ◽  
Signal Pathway ◽  
Target Protein ◽  
Inflammatory Factors ◽  
Oral Glucose ◽  
The Metabolic Syndrome

Abstract Background Metabolic syndrome is associated with obesity, inflammation, and insulin resistance. Patients with metabolic syndrome have a higher risk of turning into type II diabetes and cardiovascular disease. The metabolic syndrome has become an urgent public health problem. Insulin resistance in obesity is the common pathophysiological basis of metabolic syndrome. The insulin resistance is induced by the increasing levels of inflammatory factors during obesity. Therefore, developing a therapeutic strategy for preventing inflammation-induced insulin resistance has great significance for the treatment of metabolic syndrome. Dihydromyricetin, as a bioactive polyphenol, has been used for anti-inflammatory, anti-tumor, and improving insulin sensitivity. However, the target of DHM and the molecular mechanism of DHM in preventing inflammation-induced insulin resistance are still unclear. Methods In this study, we first confirmed the role of dihydromyricetin in inflammation-induced insulin resistance through ELISA, oral glucose tolerance test and glucose uptake test. Then, we demonstrated the pathway of dihydromyricetin ameliorated inflammation-induced insulin resistance by using signal pathway blockers, Ca2 + probes, and immunofluorescence. Finally, we clarified the target protein of dihydromyricetin by using drug affinity responsive target stability (DARTS) assay, qPCR, and western blotting. Results In this study, we first confirmed that dihydromyricetin ameliorated inflammation-induced insulin resistance in vivo and in vitro. Then, we demonstrated that dihydromyricetin ameliorated inflammation-induced insulin resistance by activating Ca2+-CaMKK-AMPK signal pathway. Finally, we clarified that dihydromyricetin activated Ca2+-CaMKK-AMPK signaling pathway by interacting with phospholipase C (PLC), its target protein. Conclusions Our results not only demonstrated that dihydromyricetin ameliorated inflammation-induced insulin resistance via the PLC-CaMKK-AMPK signal pathway but also discovered that the target protein of dihydromyricetin is PLC. Our results provided experimental data for the development of dihydromyricetin as a functional food additive and a new therapeutic strategy for treating or preventing insulin resistance and metabolic syndrome.

Carbenoxolone treatment attenuates symptoms of metabolic syndrome and atherogenesis in obese, hyperlipidemic mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1517-E1528 ◽  
Author(s):  
Alli M. Nuotio-Antar ◽  
David L. Hachey ◽  
Alyssa H. Hasty
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Body Fat ◽  
Fat Mass ◽  
Severe Obesity ◽  
Plasma Lipids ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Body Fat Mass

Glucocorticoids, which are well established to regulate body fat mass distribution, adipocyte lipolysis, hepatic gluconeogenesis, and hepatocyte VLDL secretion, are speculated to play a role in the pathology of metabolic syndrome. Recent focus has been on the activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which is capable of regenerating, and thus amplifying, glucocorticoids in key metabolic tissues such as liver and adipose tissue. To determine the effects of global 11β-HSD1 inhibition on metabolic syndrome risk factors, we subcutaneously injected “Western”-type diet-fed hyperlipidemic mice displaying moderate or severe obesity [LDL receptor (LDLR)-deficient (LDLR−/−) mice and mice derived from heterozygous agouti ( A y /a) and homozygous LDLR−/− breeding pairs ( A y /a;LDLR−/− mice)] with the nonselective 11β-HSD inhibitor carbenoxolone for 4 wk. Body composition throughout the study, end-point fasting plasma, and extent of hepatic steatosis and atherosclerosis were assessed. This route of treatment led to detection of high levels of carbenoxolone in liver and fat and resulted in decreased weight gain due to reduced body fat mass in both mouse models. However, only A y /a;LDLR−/− mice showed an effect of 11β-HSD1 inhibition on fasting insulin and plasma lipids, coincident with a reduction in VLDL due to mildly increased VLDL clearance and dramatically decreased hepatic triglyceride production. A y /a;LDLR−/− mice also showed a greater effect of the drug on reducing atherosclerotic lesion formation. These findings indicate that subcutaneous injection of an 11β-HSD1 inhibitor allows for the targeting of the enzyme in not only liver, but also adipose tissue, and attenuates many metabolic syndrome risk factors, with more pronounced effects in cases of severe obesity and hyperlipidemia.

scholarly journals Serum Fibroblast Growth Factor 21 Levels Are Positively Associated with Metabolic Syndrome in Patients with Type 2 Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Ruo-Yao Gao ◽  
Bang-Gee Hsu ◽  
Du-An Wu ◽  
Jia-Sian Hou ◽  
Ming-Chun Chen
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Body Fat ◽  
Fat Mass ◽  
Density Lipoprotein ◽  
Fibroblast Growth Factor 21 ◽  
Body Fat Mass ◽  
Fibroblast Growth

Background. Fibroblast growth factor 21 (FGF21) acts as a potent metabolic regulator. Serum FGF21 levels were significantly higher in obesity and type 2 diabetes mellitus (T2DM) populations. The aim of this study was to evaluate the relationship between serum FGF21 levels and metabolic syndrome (MetS) in T2DM patients. Methods. Fasting blood samples were obtained from 126 T2DM patients. MetS and its components were defined according to the diagnostic criteria from the International Diabetes Federation. Serum FGF21 concentrations were measured using a commercially available enzyme-linked immunosorbent assay. Results. Among these patients, 84 (66.7%) had MetS. Female gender, hypertension, systolic blood pressure (SBP), diastolic blood pressure (DBP), waist circumference (WC), body weight (BW), body mass index (BMI), body fat mass, fasting glucose, glycated hemoglobin level (HbA1c), triglyceride level (TG), urine albumin-to-creatinine ratio (UACR), insulin level, homeostasis model assessment of insulin resistance (HOMA-IR), and FGF21 levels were higher, whereas high-density lipoprotein cholesterol level (HDL-C) and estimated glomerular filtration rate (eGFR) were lower in DM patients with MetS. Univariate linear analysis revealed that hypertension, BMI, WC, body fat mass, SBP, DBP, logarithmically transformed TG (log-TG), low-density lipoprotein cholesterol (LDL-C) level, log-glucose, log-creatinine, log-UACR, log-insulin, and log-HOMA-IR positively correlated, whereas HDL-C and eGFR negatively correlated with serum FGF21 levels in T2DM patients. Multivariate forward stepwise linear regression analysis revealed that body fat mass (adjusted R2 change = 0.218; P=0.008) and log-TG (adjusted R2 change = 0.036; P<0.001) positively correlated, whereas eGFR (adjusted R2 change = 0.033; P=0.013) negatively correlated with serum FGF21 levels in T2DM patients. Conclusions. This study showed that higher serum FGF21 levels were positively associated with MetS in T2DM patients and significantly positively related to body fat mass and TG but negatively related to eGFR in these subjects.

Erythrocyte sodium/lithium countertransport is associated with thrombotic and fibrinolytic factors in 58-year-old men

2004 ◽  
Vol 91 (06) ◽  
pp. 1152-1157
Author(s):  
Lena Bokemark ◽  
Björn Fagerberg ◽  
Hans Herlitz
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Fat ◽  
Plasma Insulin ◽  
Univariate Analysis ◽  
Serum Triglyceride ◽  
Separate Analysis ◽  
The Metabolic Syndrome ◽  
Erythrocyte Sodium ◽  
Old Men

SummaryThe metabolic syndrome, in which insulin resistance is the core feature, is associated both with dysregulation of thrombosis/ fibrinolysis and erythrocyte sodium/lithium countertransport (SLC).To investigate this further we designed a cross-sectional study to examine whether factors involved in coagulationand fibrinolysis systems were associated with SLC independently of insulin resistance in 93 58-year-old men. SLC was in univariate analysis positively correlated with PAI-1 activity (r = 0.35, p <0.01), tPA antigen (r = 0.38, p <0.01), von Willebrand factor (r = 0.25, p <0.05), protein S (r = 0.26, p <0.05), and C (r = 0.30, p <0.01), and negatively associated with tPA activity(r = −0.28, p <0.01). Since these correlations could be influenced by the components of the metabolic syndrome itself, a separate analysis with adjustment for glucose infusion rate (GIR), plasma insulin, body fat, sagittal diameter of the abdomen (SD) and log serum triglyceride concentration (TG) was conducted. Then SLC was associated with tPA antigen independent of GIR, plasma insulin, body fat, SD and TG. SLC was also associated with protein C independent of GIR, insulin, body fat and SD but not TG. In conclusion, we found a relationship between SLC and the fibrinolytic system that was not related to the metabolic syndrome.

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