Laparoscopic sleeve gastrectomy ameliorates mRNA expression of inflammation-related genes in subcutaneous adipose tissue but not in peripheral monocytes of obese patients

Trachta, Pavel; Dostálová, I; Haluzíková, D; Kasalický, M; Kaválková, Petra; Drápalová, J.; Urbanová, Marie; Lacinová, Z; Mráz, Miloš; Haluzı́k, Martin

doi:10.1016/j.mce.2013.11.013

Cited by 36 publications

(26 citation statements)

References 26 publications

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“…We similarly observed no significant reductions in pro-inflammatory gene expression, at either one or 12 months after surgery, as reported herein, and in another recent study comparing 7% weight loss from RYGB versus an intensive lifestyle intervention [28]. Furthermore, in contrast to Cancello et al [46], Trachta and colleagues [22] reported that the expression of CD68 in adipose tissue, a marker of cells of the myeloid lineage, increased. Likewise, Viardot and colleagues [26] observed an increase in the number of granulocytes and Th1 cells in adipose tissue following bariatric surgery.…”

Section: Discussionsupporting

confidence: 85%

“…Paradoxically, however, while Xu et al [44] observed improvements at three months after surgery in circulating high-molecular weight adiponectin and 5′ adenosine monophosphate-activated protein kinase (AMPK) activation, along with reductions in malonyl-CoA and oxidative stress in subcutaneous adipose tissue, there were no changes in the expression of inflammatory markers. In addition, two other studies involving morbidly obese bariatric surgery patients observed no significant reductions in the expression of TNFα or IL-6, along with several other key pro-inflammatory markers at either six or 12 months after surgery [21, 22]. We similarly observed no significant reductions in pro-inflammatory gene expression, at either one or 12 months after surgery, as reported herein, and in another recent study comparing 7% weight loss from RYGB versus an intensive lifestyle intervention [28].…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, patients at this stage have lost substantial body weight [5]. Similarly, subcutaneous adipose tissue expression of CRP, IL-6, TNFα, and many other pro-inflammatory genes have been shown to decline six months after surgery [20–22, 26, 27]. However, the onset of metabolic improvements associated with bariatric/metabolic surgery is rapid, usually within days [5, 19].…”

Section: Introductionmentioning

confidence: 99%

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The short-term and long-term effects of bariatric/metabolic surgery on subcutaneous adipose tissue inflammation in humans

et al. 2017

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Context The mechanisms mediating the short- and long-term improvements in glucose homeostasis following bariatric/metabolic surgery remain incompletely understood. Objective To investigate whether a reduction in adipose tissue inflammation plays a role in the metabolic improvements seen after bariatric/metabolic surgery, both in the short-term and longer-term. Design Fasting blood and subcutaneous abdominal adipose tissue were obtained before (n=14), at one month (n=9), and 6–12 months (n=14) after bariatric/metabolic surgery from individuals with obesity who were not on insulin or anti-diabetes medication. Adipose tissue inflammation was assessed by a combination of whole-tissue gene expression and flow cytometry-based quantification of tissue leukocytes. Results One month after surgery, body weight was reduced by 13.5±4.4 kg (p<0.001), with improvements in glucose tolerance reflected by a decrease in area-under-the-curve (AUC) glucose in 3-h oral glucose tolerance tests (−105±98 mmol/L*min; p=0.009) and enhanced pancreatic β-cell function (insulinogenic index: +0.8±0.9 pmol/mmol; p=0.032), but no change in estimated insulin sensitivity (Matsuda insulin sensitivity index [ISI]; p=0.720). Furthermore, although biomarkers of systemic inflammation and pro-inflammatory gene expression in adipose tissue remained unchanged, the number of neutrophils increased in adipose tissue 15–20 fold (p<0.001), with less substantial increases in other leukocyte populations. By the 6–12 month follow-up visit, body weight was reduced by 34.8±10.8 kg (p<0.001) relative to baseline, and glucose tolerance was further improved (AUC glucose −276±229; p<0.001) along with estimated insulin sensitivity (Matsuda ISI: +4.6±3.2; p<0.001). In addition, improvements in systemic inflammation were reflected by reductions in circulating C-reactive protein (CRP; −2.0±5.3 mg/dL; p=0.002), and increased serum adiponectin (+1,358±1,406 pg/mL; p=0.003). However, leukocyte infiltration of adipose tissue remained elevated relative to baseline, with pro-inflammatory cytokine mRNA expression unchanged, while adiponectin mRNA expression trended downward (p=0.069). Conclusion Both the short- and longer-term metabolic improvements following bariatric/metabolic surgery occur without significant reductions in measures of adipose tissue inflammation, as assessed by measuring the expression of genes encoding key mediators of inflammation and by flow cytometric immunophenotyping and quantification of adipose tissue leukocytes.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The short-term and long-term effects of bariatric/metabolic surgery on subcutaneous adipose tissue inflammation in humans

et al. 2017

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“…Dietary restriction-based weight loss studies have been inconsistent in the amount of weight loss and improvement in insulin sensitivity achieved. In contrast, surgical weight loss interventions have demonstrated unique efficacy in inducing rapid, massive weight loss, along with marked improvements in metabolic health and reductions in systemic inflammation (67, 181, 199–202, 325, 368, 468, 489, 491, 527) regardless of the type of bariatric surgery (gastric banding, vertical sleeve gastrectomy, or Roux-en-Y gastric bypass). Notably, metabolic improvements following surgery typically appear within days, and well before significant weight loss, which has prompted investigation into weight loss-independent mechanisms that might be driving the improvements in glucose homeostasis.…”

Section: Adipose Tissue Inflammation and Insulin Resistancementioning

confidence: 99%

Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

Burhans

Hagman

Kuzma

et al. 2018

Comprehensive Physiology

263

241

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The objective of this comprehensive review is to summarize and discuss the available evidence of how adipose tissue inflammation affects insulin sensitivity and glucose tolerance. Low-grade, chronic adipose tissue inflammation is characterized by infiltration of macrophages and other immune cell populations into adipose tissue, and a shift towards more pro-inflammatory subtypes of leukocytes. The infiltration of pro-inflammatory cells in adipose tissue is associated with an increased production of key chemokines such as C-C motif chemokine ligand 2, pro-inflammatory cytokines including tumor necrosis factor α and interleukins 1β and 6, as well as reduced expression of the key insulin sensitizing adipokine, adiponectin. In both rodent models and humans, adipose tissue inflammation is consistently associated with excess fat mass and insulin resistance. In humans, associations with insulin resistance are stronger and more consistent for inflammation in visceral as opposed to subcutaneous fat. Further, genetic alterations in mouse models of obesity that reduce adipose tissue inflammation are – almost without exception - associated with improved insulin sensitivity. However, a dissociation between adipose tissue inflammation and insulin resistance can be observed in very few rodent models of obesity as well as in humans following bariatric surgery- or low-calorie diet-induced weight loss, illustrating that the etiology of insulin resistance is multifactorial. Taken together, adipose tissue inflammation is a key factor in the development of insulin resistance and type 2 diabetes in obesity, along with other factors that likely include inflammation and fat accumulation in other metabolically active tissues.

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“…by short-term caloric restriction or in the first weeks after a bariatric procedure (Mraz et al 2011, Trachta et al 2014. Moreover, subjects with severely depleted fat reserves as seen in mental anorexia also show increased production of proinflammatory adipokines (Dolezalova et al 2007).…”

Section: At As Immune Organmentioning

confidence: 99%

The role of adipose tissue immune cells in obesity and low-grade inflammation

Mráz

Haluzı́k

2014

Journal of Endocrinology

437

323

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Adipose tissue (AT) lies at the crossroad of nutrition, metabolism, and immunity; AT inflammation was proposed as a central mechanism connecting obesity with its metabolic and vascular complications. Resident immune cells constitute the second largest AT cellular component after adipocytes and as such play important roles in the maintenance of AT homeostasis. Obesity-induced changes in their number and activity result in the activation of local and later systemic inflammatory response, marking the transition from simple adiposity to diseases such as type 2 diabetes mellitus, arterial hypertension, and ischemic heart disease. This review has focused on the various subsets of immune cells in AT and their role in the development of AT inflammation and obesity-induced insulin resistance.

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Laparoscopic sleeve gastrectomy ameliorates mRNA expression of inflammation-related genes in subcutaneous adipose tissue but not in peripheral monocytes of obese patients

Cited by 36 publications

References 26 publications

The short-term and long-term effects of bariatric/metabolic surgery on subcutaneous adipose tissue inflammation in humans

The short-term and long-term effects of bariatric/metabolic surgery on subcutaneous adipose tissue inflammation in humans

Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

The role of adipose tissue immune cells in obesity and low-grade inflammation

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