Risks and Benefits of Sweet Pee

Läng, Florian

doi:10.1681/asn.2010091006

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…SGLT1 is expressed in intestinal epithelial cells and SGLT1 as well as SGLT2 in renal epithelial cells thus accomplishing the concentrative cellular uptake of glucose from the intestinal or renal tubular lumen across the apical cell membrane [9,13]. The low luminal glucose concentrations provide some protection against luminal bacterial growth and genetic or pharmacological inhibition of the carriers may favor the development of urinary tract infection [14,15] and diarrhea [16,17]. SGLT1 expression is, however, not restricted to renal and intestinal epithelia [18], but has also been observed in heart [18,19], lung [18], liver [18], tumor cells [20][21][22][23][24][25][26][27] and lymphocytes [28].…”

Section: Introductionmentioning

confidence: 99%

SGLT1 Deficiency Turns Listeria Infection into a Lethal Disease in Mice

Sharma

Khairnar

Madunić

et al. 2017

Cell Physiol Biochem

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Background: Cellular glucose uptake may involve either non-concentrative glucose carriers of the GLUT family or Na⁺-coupled glucose-carrier SGLT1, which accumulates glucose against glucose gradients and may thus accomplish cellular glucose uptake even at dramatically decreased extracellular glucose concentrations. SGLT1 is not only expressed in epithelia but as well in tumour cells and immune cells. Immune cell functions strongly depend on their metabolism, therefore we hypothesized that deficiency of SGLT1 modulates the defence against bacterial infection. To test this hypothesis, we infected wild type mice and gene targeted mice lacking functional SGLT1 with Listeria monocytogenes. Methods: SGLT1 deficient mice and wild type littermates were infected with 1x10⁴ CFU Listeria monocytogenes intravenously. Bacterial titers were determined by colony forming assay, SGLT1, TNF-α, IL-6 and IL-12a transcript levels were determined by qRT-PCR, as well as SGLT1 protein abundance and localization by immunohistochemistry. Results: Genetic knockout of SGLT1 (Slc5a1^–/– mice) significantly compromised bacterial clearance following Listeria monocytogenes infection with significantly enhanced bacterial load in liver, spleen, kidney and lung, and significantly augmented hepatic expression of TNF-α and IL-12a. While all wild type mice survived, all SGLT1 deficient mice died from the infection. Conclusions: SGLT1 is required for bacterial clearance and host survival following murine Listeria infection.

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