Functional microRNA screening for dietary vitamin E regulation of abdominal fat deposition in broilers.

1. Functional microRNA (miRNA) screening for abdominal fat tissue with different dietary vitamin E (VE) levels was performed to reveal miRNAs, genes and metabolic pathways involved in abdominal fat deposition in broilers. 2. A total of 240, one-day-old healthy female chicks were randomly allocated into five dietary treatments containing either 0, 20, 50, 75 or 100 IU DL-α-tocopherol acetate. The sequencing of miRNAs from abdominal fat tissues was performed. The target genes of miRNAs were predicted and enrichment analysis for these genes was performed. Diets supplemented with 50 IU VE significantly diminished abdominal fat deposition in broilers at day 35 of age. 3. A total of 29 miRNAs were differentially expressed between control and 50 IU VE treatment. Ten of the 23 target genes were enriched in four signalling pathways: tight junction, SNARE interactions in vesicular transport, regulation of autophagy and proteasome. 4. This study identified miRNA, target genes and pathways in dietary VE treatment for broilers, providing new insights into the miRNA regulation of abdominal fat deposition in broilers.

Central sympathetic control of spinal endothelin release in the rat.

Endothelin and its receptors have been identified in the spinal cord. Intrathecal administration of endothelin-3 produces hypotension in anesthetized rats. The present study was designed to identify whether endothelin-3 is released upon changes in sympathetic nervous activity. Endothelin-3-like immunoreactivity in spinal superfusates was directly correlated with resting arterial pressure. Endothelin-3 levels were enhanced by hypothalamic stimulation and by hemorrhage-induced hypotension and reduced by nitroprusside-induced hypotension. These findings suggest that sympathetic activation enhances endothelin-3 release but that nitroprusside may act directly to suppress release. We propose that endothelin-3 plays a role in spinal regulation of sympathetic outflow.

Nonadrenergic mechanisms of cocaine-induced regional vascular responses in rats.

The pressor response to cocaine is a consequence of mesenteric vasoconstriction and hindquarters vasodilation as a result of activation of alpha 1- and beta-adrenergic receptors, respectively. In the present study, evidence for additional, nonadrenergic effects of cocaine-induced changes in regional blood flow was obtained using pulsed Doppler flowmetry in conscious rats. Cocaine produced dose-dependent initial peaks (within 1 min) in mean arterial pressure concomitant with an increase in hindquarters and mesenteric vascular resistance. The sustained, modest pressor response was associated with hindquarters vasodilation and bradycardia. The cocaine-induced vasodilation was enhanced by pretreatment with indomethacin (5 mg/kg), prevented by ibuprofen (12.5 mg/kg) or 3-amino-1-[m-(trifluoromethyl)-phenyl]-2-pyrazoline (BW755C, 10.5 mg/kg) pretreatment, and unaffected by meclofenamate administration (2.5 mg/kg). Equipotent local anesthetic doses of procaine produced equivalent hindquarters vasodilator responses and more modest pressor responses. Dial-urethane anesthesia did not affect hindquarters vasodilation in response to cocaine or procaine but did reduce the mesenteric vasoconstrictor and pressor responses. These data demonstrate that the cocaine-induced hindquarters vasodilation is not mediated solely by beta-adrenergic receptors but is also dependent upon eicosanoids. Furthermore, the cocaine-induced vasodilation may be due, in part, to a direct local anesthetic effect but is not dependent upon a locomotor or behavioral stress induced increase in blood flow.