Adipokines, Inflammation, and Obesity

Clément, Karine

doi:10.1002/9783527629527.ch14

Cited by 1 publication

(3 citation statements)

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“…6 As SAT adipocytes are generally more hypertrophic than omental adipocytes, an involvement of adipocyte hypertrophy in the observed downregulation of a7nAChR, with a consequent disruption of the anti-inflammatory pathway, might be hypothesized. We also found an association between a7nAChR expression levels and adiponectin geneexpression levels in isolated adipocytes.…”

Section: Discussionmentioning

confidence: 99%

“…1 --5 This inflammatory state is characterized by an increased number of macrophages infiltrating the adipose tissue, together with an overproduction of inflammatory cytokines. 3,6 At present, factors triggering the inflammatory responses are not fully understood, especially in humans. 3,6 It is known that the neural reflexes, via the vagus nerve, can attenuate systemic inflammatory responses.…”

Section: Introductionmentioning

confidence: 99%

“…3,6 At present, factors triggering the inflammatory responses are not fully understood, especially in humans. 3,6 It is known that the neural reflexes, via the vagus nerve, can attenuate systemic inflammatory responses. 7,8 This physiological mechanism, defined as the 'cholinergic anti-inflammatory pathway', has major implications in immunology and in therapeutics.…”

Section: Introductionmentioning

confidence: 99%

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The nicotinic acetylcholine receptor α7 in subcutaneous mature adipocytes: downregulation in human obesity and modulation by diet-induced weight loss

et al. 2012

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BACKGROUND: It is known that cholinergic anti-inflammatory reflex regulates inflammation in peripheral tissues. Nicotinic acetylcholine receptors (nAChRs) are mediators of this anti-inflammatory pathway and also non-neuronal cells express functional nAChrs. A role for a7-subtype acetylcholine cholinergic receptor (a7nAChR) in insulin sensitivity improvement has already been shown in rodents both in vivo and in vitro. However, no data are available on a7nAChR expression in human adipocytes. OBJECTIVE: To investigate the expression and protein content of a7nAChR in human subcutaneous adipose tissue (SAT) and in isolated mature adipocytes. DESIGN: A total of 39 SAT biopsy specimens obtained from obese and normal-weight subjects were used to assess a7nAChR messenger RNA levels and to stimulate a7nAChR with a specific agonist and antagonist in vitro. Additional SATs from eight non-diabetic obese subjects were also studied, before and after a 3-month lifestyle intervention. RESULTS: a7nAChR expression was significantly lower in the SAT of obese subjects compared with that of normal-weight subjects. In mature adipocytes isolated from morbidly obese subjects (body mass index440 kg m À2 ), a7nAChR expression was 75% lower compared with adipocytes from normal-weight subjects. In adipocytes of obese subjects, a7nAChR was downregulated also at protein level. In eight non-diabetic obese subjects, a lifestyle intervention (3 months of diet and physical activity) induced a significant weight loss and an increase in a7nAChR SAT expression. In vitro stimulation of adipocytes with the specific a7nAChR agonist PNU282987 induced a significant anti-inflammatory effect. Furthermore, a similar downregulation of the inflammatory profile, associated with a significant increase in a7nAChR protein level, was observed after genistein stimulation. CONCLUSIONS: These results provide evidence that a7nAChR expression levels are significantly decreased in obese subjects, and that this receptor modulates inflammatory gene expression in human adipocytes. The upregulation of a7nAChR by genistein stimulation opens new insights for the management of low-grade inflammation linked to human obesity.

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Section: Discussionmentioning

confidence: 99%