Inflammatory Status is Different in Relationship to Insulin Resistance in Severely Obese People and Changes after Bariatric Surgery or Diet-induced Weight Loss

Ballesteros-Pomar, María D.; Calleja, Sara; Díez-Rodríguez, R.; Calleja-Fernández, Alicia; Vidal-Casariego, Alfonso; Núñez-Alonso, Alejandro; Cano-Rodríguez, Isidoro; Olcoz-Goñi, J.L.

doi:10.1055/s-0034-1382035

Cited by 20 publications

(17 citation statements)

References 15 publications

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“…However, the effect of EGCG on insulin resistance and its mechanism in treating NAFLD has rarely been discussed. In our study, EGCG allevi- (Table 1), as previously shown wherein weight loss induced by diet control, exercise, pharmacotherapy and bariatric surgery improves insulin resis tance [26,27] . However, more importantly, our study confirmed that an EGCG-induced increase in insulin clearance may contribute to the improvement of insulin resistance in NAFLD mice ( Figure 6).…”

Section: Discussionsupporting

confidence: 74%

Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic fatty liver disease mice

et al. 2015

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Aim: Epigallocatechin-3-gallate (EGCG) is a major polyphenol in green tea. In this study, we investigated the effects of EGCG on insulin resistance and insulin clearance in non-alcoholic fatty liver disease (NAFLD) mice. Methods: Mice were fed on a high-fat diet for 24 weeks. During the last 4 weeks, the mice were injected with EGCG (10, 20 and 40 mg·kg -1 ·d -1 , ip). Glucose tolerance, insulin tolerance and insulin clearance were assessed. After the mice were euthanized, blood samples and tissue specimens were collected. Glucose-stimulated insulin secretion was examined in isolated pancreatic islets. The progression of NAFLD was evaluated histologically and by measuring lipid contents. Insulin-degrading enzyme (IDE) protein expression and enzyme activity were detected using Western blot and immunocapture activity assays, respectively. Results: The high-fat diet significantly increased the body weight and induced grade 2 or 3 liver fatty degeneration (steatosis, lobular inflammation and ballooning) accompanied by severe hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in the model mice. Administration of EGCG dose-dependently ameliorated the hepatic morphology and function, reduced the body weight, and alleviated hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in NAFLD mice. Furthermore, EGCG dosedependently enhanced insulin clearance and upregulated IDE protein expression and enzyme activity in the liver of NAFLD mice. Conclusion: EGCG dose-dependently improves insulin resistance in NAFLD mice not only by reducing body weight but also through enhancing the insulin clearance by hepatic IDE. The results suggest that IDE be a potential drug target for the treatment of NAFLD.

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Section: Discussionsupporting

confidence: 74%

Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic fatty liver disease mice

et al. 2015

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“…Aside from morbid obesity, total NK cell counts have been reported in the peripheral blood of donors with insulin resistance and have declined following weight reduction, suggesting an immune metabolic disorder. Because CD56 bright NK cells were less numerous (data not shown), our results focused on circulating cytotoxic CD56 dim cells.…”

Section: Resultsmentioning

confidence: 99%

Insulin signaling as a potential natural killer cell checkpoint in fatty liver disease

Amer

Salhab

Noureddin

et al. 2018

Hepatology Communications

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Insulin resistance is a key risk factor in the progression of nonalcoholic fatty liver disease (NAFLD) and may lead to liver fibrosis. Natural killer (NK) cells are thought to exert an antifibrotic effect through their killing of activated hepatic stellate cells (HSCs). Here, we investigated how the interplay between NK cells and HSCs are modified by insulin resistance in NAFLD. Fresh peripheral blood NK cells (clusters of differentiation [CD]56dim, CD16+) were collected from 22 healthy adults and 72 patients with NAFLD not currently taking any medications and without signs of metabolic syndrome. NK cells were assessed for insulin receptor expressions and cytotoxic activity when cultured in medium with HSCs. Fibrosis severities in patients with NAFLD were correlated linearly with elevated serum proinflammatory cytokine expression and insulin resistance severity. At the same time, fibrosis severities inversely correlated with insulin receptor expressions on NK cells as well as with their cytotoxic activities determined by CD107a by flow cytometry. NK cells from donors exhibiting severe fibrosis and insulin resistance exhibited significant mammalian target of rapamycin and extracellular signal‐regulated kinase depletion (through NK cell western blot quantitation), increased apoptosis, and failure to attenuate HSC activation in vitro. While exposure to insulin stimulated the cytotoxic activity of healthy NK cells, rapamycin prevented this effect and reduced NK insulin receptor expressions. Conclusion: Elevated insulin levels in F1 and F2 fibrosis enhances NK cell cytotoxic activity toward HSCs and prevents fibrosis progression by insulin receptors and downstream mammalian target of rapamycin and extracellular signal‐regulated kinase pathways. At more advanced stages of insulin resistance (F3 and F4 fibrosis), impaired NK cell activity rooted in low insulin receptor expression and or low serum insulin levels could further deteriorate fibrosis and may likely lead to cirrhosis development. (Hepatology Communications 2018;2:285‐298)

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“…The lack of a clear cut-off for defining IR in children and adolescents is also a problem [6]. Moreover the results of the recently published studies point to significant differences between pediatric and adult mechanisms of the IR development, the close correlation between IR and immune status and thyroid function [8][9][10]. A novel insight into these problems is possible since the analysis of the expression of central obesity (CO) and Type 2 Diabetes Mellitus genes has became achievable [11][12][13][14][15].…”

Section: Methodsmentioning

confidence: 99%

Expression of the Central Obesity and Type 2 Diabetes Mellitus Genes is Associated with Insulin Resistance in Young Obese Children

Skoczeń

Wójcik

Fijorek

et al. 2015

Exp Clin Endocrinol Diabetes

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Inflammatory Status is Different in Relationship to Insulin Resistance in Severely Obese People and Changes after Bariatric Surgery or Diet-induced Weight Loss

Abstract: NK cells are significantly increased in IR severely obese people in respect to IS, suggesting a slightly different immune status in these patients with a probable dietary relationship. Weight loss could reverse this increase either after VLCD or after bariatric surgery.

Cited by 20 publications

References 15 publications

Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic fatty liver disease mice

Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic fatty liver disease mice

Insulin signaling as a potential natural killer cell checkpoint in fatty liver disease

Expression of the Central Obesity and Type 2 Diabetes Mellitus Genes is Associated with Insulin Resistance in Young Obese Children

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