title: SGLT1 protein expression in plasma membrane of acinar cells correlates with the sympathetic outflow to salivary glands in diabetic and hypertensive rats.
abstract: Salivary gland dysfunction is a feature in diabetes and hypertension. We hypothesized that sodium-glucose cotransporter 1 (SGLT1) participates in salivary dysfunctions through a sympathetic- and protein kinase A (PKA)-mediated pathway. In Wistar-Kyoto (WKY), diabetic WKY (WKY-D), spontaneously hypertensive (SHR), and diabetic SHR (SHR-D) rats, PKA/SGLT1 proteins were analyzed in parotid and submandibular glands, and the sympathetic nerve activity (SNA) to the glands was monitored. Basal SNA was threefold higher in SHR (P < 0.001 vs. WKY), and diabetes decreased this activity (∼50%, P < 0.05) in both WKY and SHR. The catalytic subunit of PKA and the plasma membrane SGLT1 content in acinar cells were regulated in parallel to the SNA. Electrical stimulation of the sympathetic branch to salivary glands increased (∼30%, P < 0.05) PKA and SGLT1 expression. Immunohistochemical analysis confirmed the observed regulations of SGLT1, revealing its location in basolateral membrane of acinar cells. Taken together, our results show highly coordinated regulation of sympathetic activity upon PKA activity and plasma membrane SGLT1 content in salivary glands. Furthermore, the present findings show that diabetic- and/or hypertensive-induced changes in the sympathetic activity correlate with changes in SGLT1 expression in basolateral membrane of acinar cells, which can participate in the salivary glands dysfunctions reported by patients with these pathologies.
authors.affiliation: Dept. of Physiology and Biophysics, Univ. of Sao Paulo, Sao Paulo, Brazil.
authors.forename: Robinson
authors.initials: R
authors.lastname: Sabino-Silva
authors.forename: Ana B T
authors.initials: AB
authors.lastname: Alves-Wagner
authors.forename: Katia
authors.initials: K
authors.lastname: Burgi
authors.forename: Maristela M
authors.initials: MM
authors.lastname: Okamoto
authors.forename: Adilson S
authors.initials: AS
authors.lastname: Alves
authors.forename: Guilherme A
authors.initials: GA
authors.lastname: Lima
authors.forename: Helayne S
authors.initials: HS
authors.lastname: Freitas
authors.forename: Vagner R
authors.initials: VR
authors.lastname: Antunes
authors.forename: Ubiratan F
authors.initials: UF
authors.lastname: Machado
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D002462:Cell Membrane / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000503:physiopathology; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D010306:Parotid Gland / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D015398:Signal Transduction; D051269:Sodium-Glucose Transporter 1 / Q000378:metabolism*; D013363:Submandibular Gland / Q000378:metabolism* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000378:metabolism* / Q000503:physiopathology
chemical_list: C495676:Slc5a1 protein, rat; D051269:Sodium-Glucose Transporter 1; D017868:Cyclic AMP-Dependent Protein Kinases