The effect of insulin resistance and exercise on the percentage of CD16⁺ monocyte subset in obese individuals

Abstract

Obesity is now considered to be an inflammatory condition associated with many pathological consequences, including insulin resistance. It is proposed that insulin resistance contributes to the aggravation of the inflammatory dysfunction in obesity. The effect of obesity on the percentage of monocytes was previously observed in class II and III obese individuals who presented other alterations in addition to insulin resistance. In this study we observed that insulin-resistant obese individuals, but not insulin-sensitive ones, had an increased percentage of CD14(+) CD16(+) monocytes. This fact shows that a dysfunction of the monocyte percentage in class I obese individuals is only seen when this condition is associated with insulin resistance.

Analysis of the percentages of monocyte subsets and ILC2s, their relationships with metabolic variables and response to hypocaloric restriction in obesity

“…We found a positive relationship between insulin-resistance and NCMs, suggesting that obesity-induced insulin resistance aggravates the chronic low-grade inflammation favoring the shift to increase the CD14 -CD16 ++ subset (NCM) [21,49]. We also confirmed the relations of NCMs and ILC2s with plasma lipids.…”

“…The minor CD16 + Mo subpopulation comprises the remaining 10-15% and is subdivided further into intermediate monocytes (IM; CD14 + CD16 + ) and non-classical monocytes (NCM; CD14 -CD16 ++ ), both with a pro-inflammatory phenotype and are elevated in chronic inflammatory and metabolic diseases [12][13][14][15][16][17][18]. Changes in monocytes subsets CD14 ++ CD16 -, CD14 + CD16 + and CD14 -CD16 ++ have been described after dietary interventions in obese individuals [19][20][21][22]. Monocytes can migrate toward AT and endothelium, where they become converted into macrophages.…”

The continuum of monocyte phenotypes: Experimental evidence and prognostic utility in assessing cardiovascular risk

“…Exercise training for 12 weeks in healthy physically inactive older adults reduced the percentage of CD14 + CD16 + (intermediate) monocytes in circulation compared with baseline, possibly through exercise‐induced transient spikes in endogenous cortisol levels . A small study shows that insulin‐resistant obese individuals, but not insulin‐sensitive ones, have an increased percentage of CD14 + CD16 + monocytes, which is reduced 1 h after an aerobic exercise session compared with baseline, along with an increase in the absolute monocyte count, suggesting that distribution of monocyte subsets undergoes dynamic changes even within short time frames . Another recent study on 136 patients suggests an association among CD14 − CD16 + monocytes above 8% at hospital discharge, higher fat deposition in the gluteofemoral or gynoid area, and reduction of rehospitalization for heart failure …”

<p>The Exercise Training Modulatory Effects on the Obesity-Induced Immunometabolic Dysfunctions</p>

“…[167][168][169] Furthermore, recent investigations on humans have revealed the provocation of mechanisms associated with M2 markers following exercise. 170,171 Additionally, the improvement of chemotactic status, leukocyte functions, 171,172 MONs differentiation, 92,173 insulin sensitivity, 174 the reduction of inflammatory markers, metabolic health-related risk factors, [174][175][176] and circulating inflammatory MONs 11,12 emerge following different exercise training protocols. In fact, the beneficial impacts of exercise training are induced by both immune and metabolic-related cells, such as adipocytes, hepatocytes, and myocytes.…”