scholarly journals Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats

2021 ◽  
Vol 8 ◽  
Author(s):  
Sanja Kovačević ◽  
Jelena Brkljačić ◽  
Danijela Vojnović Milutinović ◽  
Ljupka Gligorovska ◽  
Biljana Bursać ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Energy Intake ◽  
Visceral Adipose Tissue ◽  
Insulin Signaling ◽  
Metabolic Disorders ◽  
Male Rats ◽  
Plasma Uric Acid ◽  
Visceral Adipose

Introduction: Obesity and related metabolic disturbances are frequently related to modern lifestyle and are characterized by excessive fructose intake. Visceral adipose tissue (VAT) inflammation has a central role in the development of insulin resistance, type 2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility and progression of metabolic disorders are not yet fully understood, our aim was to examine inflammation and insulin signaling in VAT of fructose-fed female and male adult rats.Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake, VAT mass and histology, and systemic insulin sensitivity. VAT insulin signaling and markers of VAT inflammation, and antioxidative defense status were also evaluated.Results: The fructose diet had no effect on VAT mass and systemic insulin signaling in the female and male rats, while it raised plasma uric acid, increased PPARγ level in the VAT, and initiated the development of a distinctive population of small adipocytes in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFκB, increased expression of proinflammatory cytokines (IL-1β, IL-6, and TNFα), and protein level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase. In contrast to the females, the fructose diet had no effect on plasma uric acid and VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling were observed.Conclusion: Even though dietary fructose did not elicit changes in energy intake and led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable of storing fats further. In contrast to the males, this state of VAT was accompanied with enhanced inflammation, which most likely contributed to the development of insulin resistance. The observed distinction could possibly originate from sex-related differences in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor for the development of T2D. Our results emphasize that adipose tissue dysfunction, rather than its simple enlargement, could significantly contribute to the onset and development of obesity and related metabolic disorders.

scholarly journals Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

2020 ◽  
Author(s):  
Luisa Fernández-Chirino ◽  
Neftali Eduardo Antonio-Villa ◽  
Arsenio Vargas-Vázquez ◽  
Paloma Almeda-Valdés ◽  
Donají Gómez-Velasco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Visceral Adipose Tissue ◽  
Visceral Obesity ◽  
Causal Mechanism ◽  
Mediation Analyses ◽  
Bidirectional Relationship ◽  
Visceral Adipose

BACKGROUND: Serum uric acid (SUA) has a relationship with cardiometabolic conditions such as insulin resistance (IR) and visceral adipose tissue (VAT) accumulation. Here, we aimed to clarify the nature of this relationship and the underlying causality mechanism. METHODS: We conducted a population-based cross-sectional study comprising 8,504 subjects joining both NHANES 2003-2004 and 2011-2012 cycles and ENSANUT Medio Camino 2016. We performed mixed effects linear regression models using HOMA2-IR, adipoIR, and METS-VF as indicators of IR and VAT accumulation. Furthermore, we performed mediation analyses to assess a potential causal mechanism and ROC curves to establish cut-off points for identification of IR and visceral obesity using SUA. Finally, with an additional dataset comprised of 226 subjects with both euglycemic hyperinsulinemic clamp (EHC) and dual X-ray absorptiometry (DXA) measurements for IR and VAT accumulation, we performed a network of confirmatory mediation analyses. RESULTS:We found that SUA has a mediating role inside the bidirectional relationship between IR and visceral obesity, and it is part of an underlying causality mechanism which includes adiponectin. The proportion of the mechanism mediated by SUA is greater when stated that IR (in either peripheral or adipose tissue) leads to VAT accumulation (14.90%[13.20%-17.00%] and 15.54%[13.61% - 18.00%] to 4.88%[3.06%-7.00%] and 8.13%[5.91% - 10.00%]) instead of the opposite direction. This result was confirmed by mediation analyses using gold-standard measurements. CONCLUSIONS:Elevated SUA acts as mediator inside the bidirectional relationship between IR andVAT accumulation. Its role appears to be larger when considering adipose tissue IR as the promoter for VAT accumulation.

scholarly journals Effect of Insulin Resistance on Lipolytic activity of Adipose Tissue in Male Rats

2012 ◽  
Vol 1 (2) ◽  
pp. 68-73
Author(s):  
R Eldeeb ◽  
MH Gamal-Eldin ◽  
EA Khowailed ◽  
MM Fathy ◽  
N Shantakumari ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Body Weight ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Lipolytic Activity ◽  
Fasting Blood Glucose ◽  
Significant Rise ◽  
Male Rats ◽  
Visceral Adipose

Background: The excess usage of fructose as a sweetener has raised the incidence of insulin resistance among the population which is associated with dyslipedemia, hypertension and obesity. This work studied the effect of induced insulin resistance on body weight, blood pressure, lipid profile, glycemic state and lipolytic activity of adipose tissue in male rats. Methods: Twenty male rats of 129.4 g average body weight (BW) were divided equally into two groups. Both had free access to water. The control group had pure water; the experimental group had water mixed with 25% of fructose to induce insulin resistance. After 3 months body weight, blood pressure, fasting blood glucose, insulin levels, lipid profile of both groups were measured and lipolytic activity of adipose tissue was assessed. Results: Rats given fructose for 3 months showed significant increase in BW, systolic blood pressure, triglyceride, Cholesterol, low density lipoprotein, fasting blood glucose and insulin levels with a significant decline in highdensity lipoprotein. Lipolytic activity of subcutaneous (SC) and visceral adipose tissue in presence of adrenaline increased significantly which runs in parallel with the results obtained in presence of insulin as it showed a significant rise in both SC and visceral adipose tissue. Data were considered statistically significant at alpha level of 5%. Conclusion: Insulin resistance induced in male rat by high fructose consumption showed a significant rise in BW and is associated with hypertension and dyslipidemia with significant rise in lipolytic activity of both SC and visceral adipose tissue. DOI: http://dx.doi.org/10.3126/njms.v1i2.6602 Nepal Journal of Medical Sciences. 2012;1(2): 68-73

scholarly journals Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

2022 ◽  
Author(s):  
Luisa Fernández‐Chirino ◽  
Neftali Eduardo Antonio‐Villa ◽  
Carlos A. Fermín‐Martínez ◽  
Alejandro Márquez‐Salinas ◽  
Enrique C. Guerra ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Visceral Adipose Tissue ◽  
Elevated Serum ◽  
Visceral Adipose

scholarly journals Elevated Serum Uric Acid Is a Facilitating Mechanism for Insulin Resistance Mediated Accumulation of Visceral Adipose Tissue

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A44-A45
Author(s):  
Luisa Fernandez-Chirino ◽  
Neftali Eduardo Antonio-Villa ◽  
Omar Yaxmehen Bello-Chavolla ◽  
Paloma Almeda-Valdes
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Visceral Adipose Tissue ◽  
Visceral Obesity ◽  
Mediation Analyses ◽  
Bidirectional Relationship ◽  
Males And Females ◽  
Visceral Adipose

Abstract Background: Serum uric acid (SUA) is related to cardiometabolic conditions such as insulin resistance (IR) and visceral adipose tissue (VAT) accumulation, which have a thoroughly explored bidirectional relationship. Here, we aimed to clarify the nature of the role uric acid plays inside this relationship, alongside the underlying causality mechanism. Methods: We conducted a population-based cross-sectional study comprising 8,504 subjects from a joint cohort composed from both NHANES 2003–2004 and 2011–2012 cycles and ENSANUT Medio Camino 2016. We performed mixed effects linear regression models using HOMA2-IR, adipoIR, and METS-VF as indicators of both peripheral and adipose tissue IR and VAT accumulation, indicating the subject’s cohort of origin as a random effect. Furthermore, we performed multiple mediation analyses to assess a potential causal mechanism and ROC curves to establish cut-off points for identification of IR and visceral obesity using SUA. Finally, with an additional dataset comprised of 226 subjects with both euglycemic hyperinsulinemic clamp (EHC) and dual X-ray absorptiometry (DXA) measurements for IR and VAT accumulation, we performed a network of confirmatory mediation analyses including adiponectin measurements. Results: We found that SUA has a mediating role inside the bidirectional relationship between IR and visceral obesity, and it is part of an underlying causality mechanism which includes adiponectin. The proportion of the mechanism mediated by SUA is greater when stated that IR (in either peripheral or adipose tissue) leads to VAT accumulation (14.90%[13.20%-17.00%] and 15.54%[13.61%-18.00%]) instead of the opposite direction (4.88%[3.06%-7.00%] and 8.13%[5.91%-10.00%]). This result was strengthened by a mediation analysis network using the gold-standard measurements where we observed that the joint effect of SUA and adiponectin mediated 16.32% [8.84%-26.00%] for the effect of IR and VAT accumulation and 12.52% [3.23%-23.00%] in the opposite direction. Cut-off points for SUA to predict peripheral IR were 6.1 mg/dL and 4.8 mg/dL, for males and females respectively. For visceral obesity, cut-offs were 6.4 mg/dL and 4.8 mg/dL for males and females. SUA had a high negative predictive value for all assessments. Conclusions: Elevated SUA acts as mediator inside the bidirectional relationship between IR and VAT accumulation. Its role appears to be larger when considering adipose tissue IR as the promoter for VAT accumulation.

scholarly journals Protocatechuic acids protects against high glucose- induced insulin resistance in human visceral adipose tissue

2016 ◽  
Vol 62 (5) ◽  
pp. 45-46
Author(s):  
Paulina Ormazabal ◽  
Beatrice Scazzocchio ◽  
Rosaria Varì ◽  
Annunziata Iacovelli ◽  
Roberta Masella
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Glucose ◽  
Protective Role ◽  
Insulin Sensitizer ◽  
20 Nm ◽  
Visceral Adipose

Adipocytes exposed to high glucose concentrations exhibit impaired insulin signaling. Binding of insulin to its membrane receptor activates insulin metabolic pathway leading to IRS-1 and AKT phosphorylations. The accumulation of visceral adipose tissue (VAT) correlates with insulin resistance and metabolic syndrome. Anthocyanins (ACN) are bioactive food compounds of great nutritional interest. We have shown that protocatechuic acid (PCA), a major metabolite of ACN, might exert insulin-sensitizer activities in human visceral adipose tissue. The aim of this work was to define the protective role of PCA against insulin-resistance induced by high glucose in VAT.Methodology: VAT obtained from control subject (BMI≤25) were separated in four experimental groups: i) PCA: samples treated for 24 h with 100 μM PCA, ii) GLU: VAT treated with 30 mM glucose for 24 h, iii) PCA+GLU: 1 hour incubation with 100 μM PCA before adding glucose (30 mM, 24 h), iv) CTR: vehicle. After treatment, VAT groups were (or not) acutely stimulated with insulin (20 nM, 20 min). Tyr-IRS-1 and Ser-Akt phosphorylations were assessed by Western blotting (WB) in basal or insulin stimulated tissues in all experimental groups. Samples were assessed for IRS-1, IR, Akt and GLUT4 protein content by WB. Results: No differences in protein contents between experimental groups were found. GLU tissues showed a lower increment in insulin-stimulated phosphorylation of IRS-1 and Akt compared to CTR and PCA samples. This impaired activation was completely reversed by the pretreatment with PCA.Conclusion: An in-vitro insulin-resistance condition induced by high glucose was established in biopsies of VAT. PCA restores the ability of GLU-tissues to fully respond to insulin by increasing IRS-1 and Akt phosphorylations. These results confirm the insulin-sensitizer effect of PCA on VAT previously reported by our group. An anthocyanin rich diet might help to protect against insulin-resistance in VAT.

scholarly journals Abdominal Subcutaneous and Visceral Adipose Tissue and Insulin Resistance in the Framingham Heart Study

Obesity ◽  
2010 ◽  
Vol 18 (11) ◽  
pp. 2191-2198 ◽  
Author(s):  
Sarah R. Preis ◽  
Joseph M. Massaro ◽  
Sander J. Robins ◽  
Udo Hoffmann ◽  
Ramachandran S. Vasan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Framingham Heart Study ◽  
Heart Study ◽  
Visceral Adipose

Abstract P232: Worse Cardiometabolic Health in African Immigrants than African-Americans: Reconsideration of the Healthy Immigrant Effect

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Anne E Sumner ◽  
Michelle Y O'Connor ◽  
Caroline K Thoreson ◽  
Madia Ricks ◽  
Amber B Courville ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
African Americans ◽  
Visceral Adipose Tissue ◽  
African Immigrants ◽  
Cardiometabolic Health ◽  
Sensitivity Index ◽  
Healthy Immigrant Effect ◽  
Immigrant Effect ◽  
Visceral Adipose

In decades past, African immigrants were considered to have better cardiometabolic health than African Americans. Whether this health advantage continues to exist in the 21st century is unknown. To explore differences in markers of cardiometabolic health, oral glucose tolerance tests, blood pressure (BP), visceral adipose tissue (VAT) volume and the waist circumference (WC) which predicts insulin resistance were compared in 210 men (134 African immigrants, 76 African Americans, mean age 36±9y (mean±SD), range 20-64y) who self-identified as healthy. Insulin resistance was defined by the lowest quartile of the insulin sensitivity index (SI≤2•28mU/L-1.min-1). Receiver operating characteristic curves and the Youden Index were used to identify the WC which optimally predicts insulin resistance. BMI was lower in African immigrants than African Americans (27.4±3.9 vs. 29.3±5.5kg/m2, P<0.01). Adjusting for BMI, WC did not differ between groups (93±5 vs. 94±5cm, P=0.55); but African immigrants had more visceral adipose tissue (VAT) (P<0.001) higher BP (P≤0.01), higher fasting glucose (P≤0.001) and 2h glucose (P<0.001) as well as a higher prevalence of previously undiagnosed diabetes (7% (9 of 134) vs. 0% (0 of 76), P<0.01) and pre-diabetes (35% (47 of 134) vs. 22% (17 of 76), P<0.01). Degree of insulin resistance did not differ in African immigrants and African Americans (4.17±2.88 vs. 4.24±2.61 (mU/L)-1 .min-1, P=0.88). Yet, the WC which optimally predicted insulin resistance was lower in African immigrants than African Americans, specifically 92 cm and 102 cm, respectively. As African immigrants had higher VAT, BP and glucose levels than African Americans, the healthy immigrant effect may no longer be a valid concept. As insulin resistance occurred at a lower WC in African immigrants than African Americans, lower BMI in African immigrants does not appear to provide protection from cardiometabolic risk.

scholarly journals Effects of food pattern change and physical exercise on cafeteria diet-induced obesity in female rats

2012 ◽  
Vol 108 (8) ◽  
pp. 1511-1518 ◽  
Author(s):  
Jéferson F. Goularte ◽  
Maria B. C. Ferreira ◽  
Gilberto L. Sanvitto
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Physical Exercise ◽  
Energy Intake ◽  
Liver Weight ◽  
Cafeteria Diet ◽  
Chow Diet ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Obesity affects a large number of people around the world and appears to be the result of changes in food intake, eating habits and physical activity levels. Changes in dietary patterns and physical exercise are therefore strongly recommended to treat obesity and its complications. The present study tested the hypothesis that obesity and metabolic changes produced by a cafeteria diet can be prevented with dietary changes and/or physical exercise. A total of fifty-six female Wistar rats underwent one of five treatments: chow diet; cafeteria diet; cafeteria diet followed by a chow diet; cafeteria diet plus exercise; cafeteria diet followed by a chow diet plus exercise. The duration of the experiment was 34 weeks. The cafeteria diet resulted in higher energy intake, weight gain, increased visceral adipose tissue and liver weight, and insulin resistance. The cafeteria diet followed by the chow diet resulted in energy intake, body weight, visceral adipose tissue and liver weight and insulin sensitivity equal to that of the controls. Exercise increased total energy intake at week 34, but produced no changes in the animals' body weight or adipose tissue mass. However, insulin sensitivity in animals subjected to exercise and the diet was similar to that of the controls. The present study found that exposure to palatable food caused obesity and insulin resistance and a diet change was sufficient to prevent cafeteria diet-induced obesity and to maintain insulin sensitivity at normal levels. In addition, exercise resulted in normal insulin sensitivity in obese rats. These results may help to develop new approaches for the treatment of obesity and type 2 diabetes mellitus.

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