The effects of l-arginine and l-NAME supplementation on redox-regulation and thermogenesis in interscapular brown adipose tissue

Abstract

These data suggest that nitric oxide (NO) produced by iNOS could also contribute to overall NO-associated regulation of thermogenesis in IBAT. Namely, that iNOS, i.e. NO, in correlation with enhanced thermogenesis, additionally induced IBAT hyperplasia and UCP1 level compared to that induced by low temperature. Cooperative action of decreased apoptosis accompanied by increased tissue hyperplasia and UCP1 level, observed in IBAT of cold-acclimated rats, would be a way of meeting the metabolic requirements for increased thermogenesis.

Leptin immunoexpression and innervation in rat interscapular brown adipose tissue of cold-acclimated rats: the effects of L-arginine and L-NAME.

“…In contrast, very low levels of iNOS mRNA were expressed, and cold stimulation failed to increase iNOS mRNA levels in IBAT. Our previous results are in accordance with their findings, but we also observed that L-arginine treatment of cold-acclimated rats increases iNOS expression [21]. It is possible that L-arginine treatment synergistically with cold changes expression pattern of NOSs and, at least in some part may stimulate leptin expression observed in that experimental group.…”

“…Giordano et al [16] showed existence of a noradrenalin-modulated functional NOS system in brown adipocytes nuclei. We also recently reported the nuclear positivity of brown adipocytes for iNOS [21].…”

“…Since we previously found that L-arginine additionally increases UCP1 expression in cold acclimated rats [21], it is possible that the leptin expression observed in brown adipocytes induced by L-arginine might be a stop signal for the overstimulated IBAT thermogenesis (energy expenditure higher than energy deposition). Locally, leptin may be stimulated by NO to oppose the effects of sympathetic activation and prevent overheating and/or underweight.…”

“…It is known that the SNS plays an essential role in the control of UCP1 gene expression [29]. Cold exposure activates thermogenesis by increasing noradrenaline release from sympathetic nerves, which induces UCP1 expression trough the β 3 adrenergic receptor-mediated and cAMPdependent mechanism [18,21,[30][31][32][33]. Simultaneously, also acting through the β 3 -adrenergic receptor-mediated and cAMP-dependent mechanism, sympathetic stimulation inhibits leptin expression in brown and white adipose tissues [34].…”

“…NO generation represents an important mechanism of modulating different IBAT functions, including vasodilatation of IBAT microcirculation [18], brown adipocytes proliferation [19], and mitochondriogenesis [20]. We also showed recently that the NO plays an important role in the regulation of IBAT function [21].…”