Effects of a sympathetic activation by lower body negative pressure on glucose and lipid metabolism

Abstract

The effects of a sympathetic activation elicited by a lower body negative pressure (LBNP) (at -15 mmHg for 75 min) were assessed in 7 healthy subjects on two occasions: (i) in post-absorptive conditions, and (ii) during glucose infusion (22.2 mumol kg-1 min-1). LBNP increased plasma norepinephrine concentration and heart rate. It did not alter whole-body glucose metabolism (measured with [6,6-2H]glucose) and glycerol turnover (measured with [1,1,2,3,3-2H]glycerol). Interstitial glycerol concentrations were monitored with microdialysis in subcutaneous adipose tissue and in skeletal muscle. LBNP increased dialysate glycerol concentrations in muscle by 16% (P < 0.03) but not in adipose tissue in post-absorptive conditions, and by 37% in adipose tissue (P < 0.05) but not in muscle during glucose infusion. These results indicate that an LBNP-induced sympathetic activation (i) does not increase endogenous glucose production, and (ii) induces only a slight stimulation of lipolysis in adipose tissue during glucose infusion.

Intraneural stimulation elicits an increase in subcutaneous interstitial glycerol levels in humans

“…A role for sympathetic outflow to skeletal muscle in human obesity has been proposed (Spraul et al 1993; Snitker et al 1998), but this sympathetic subdivision modulates glycerol concentrations in muscle and not in subcutaneous fat tissue (Henry et al 1998). Our present demonstration of a neural modulation of subcutaneous fat tissue metabolism mediated via cutaneous nerve fascicles, in conjunction with the well established fact that sympathetic activity at rest and in response to various stimuli differs substantially between fascicles innervating muscle and skin (Vallbo et al 1979; Wallin & Elam, 1997 a ), indicates that a sympathetically mediated mobilization of fat stores may be highly differentiated and may involve different tissues depending on the type of stimulus.…”

Effects of dexamethasone on the metabolic responses to mental stress in humans

“…In these previous studies, not only the stimulation of SNS, as documented by microneurography of the lateral peroneal nerve, but also the vasodilatory effects normally elicited by these manoeuvers were inhibited by dexamethasone. A role of the SNS in these forms of insulin resistance appears supported by the observations that noradrenergic activation elicited by a lower body negative pressure reduces acutely insulin-mediated glucose disposal (Lembo et al, 1994;Henry et al, 1998). This indicates that mental stress activates SNS through different central pathways than those stimulated by insulin, alcohol and hypoglycaemia.…”

Relationship of muscle sympathetic nerve activity to insulin sensitivity

“…A similar reduction in insulin sensitivity is seen during the administration of the α-adrenergic agonist norepinephrine [20] suggesting that the reduction in insulin sensitivity may be mediated by α1-adrenergic receptors [25]. However, other studies have not found whole body glucose uptake to be affected by sympathetic stimulation [12]. Some prospective studies suggest that sympathetic activation precedes insulin resistance: norepinephrine levels in men predict insulin levels 10 years later [24] and greater sympathetic reactivity is associated with the development of insulin resistance many years later [5].…”