AIM: We aimed to determine whether the sodium/glucose cotransporter family member SGLT3, a proposed glucose sensor, is expressed in the intestine and/or kidney, and if its expression is altered in mouse models of obesity and in humans before and after weight-loss surgery. MAIN METHODS: We used in-situ hybridization and quantitative PCR to determine whether the Sglt3 isoforms 3a and 3b were expressed in the intestine and kidney of C57, leptin-deficient ob/ob, and diabetic BTBR ob/ob mice. Western blotting and immunohistochemistry were also used to assess SGLT3 protein levels in jejunal biopsies from obese patients before and after weight-loss Roux-en-Y gastric bypass surgery (RYGB), and in lean healthy controls. KEY FINDINGS: Sglt3a/3b mRNA was detected in the small intestine (duodenum, jejunum and ileum), but not in the large intestine or kidneys of mice. Both isoforms were detected in epithelial cells (confirmed using intestinal organoids). Expression of Sglt3a/3b mRNA in duodenum and jejunum was significantly lower in ob/ob and BTBR ob/ob mice than in normal-weight littermates. Jejunal SGLT3 protein levels in aged obese patients before RYGB were lower than in lean individuals, but substantially upregulated 6 months post-RYGB. SIGNIFICANCE: Our study shows that Sglt3a/3b is expressed primarily in epithelial cells of the small intestine in mice. Furthermore, we observed an association between intestinal mRNA Sglt3a/3b expression and obesity in mice, and between jejunal SGLT3 protein levels and obesity in humans. Further studies are required to determine the possible role of SGLT3 in obesity.

• MeSH
• dospělí MeSH
• down regulace MeSH
• exprese genu MeSH
• hmotnostní úbytek MeSH
• inzulin metabolismus   MeSH
• inzulinová rezistence MeSH
• jejunum metabolismus   MeSH
• leptin nedostatek   metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• messenger RNA genetika   metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• obezita genetika   metabolismus   MeSH
• protein - isoformy MeSH
• střevní sliznice metabolismus   MeSH
• tenké střevo metabolismus   MeSH
• transkriptom MeSH
• transportní proteiny pro sodík a glukosu biosyntéza   genetika   metabolismus   MeSH
• žaludeční bypass MeSH
• zvířata MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Kardiovaskulárna choroba (KVCH) je najčastejšou príčinou úmrtia u pacienta s diabetes mellitus 2. typu (DM2T). Veľká časť chorobnej záťaže nemôže byť vysvetlená len bežnými kardiovaskulárnymi (KV) rizikovými faktormi. Populačné štúdie odhalili 80% výskyt hypertenzie u pacientov s diabetom, čo je podstatne viac, ako by sa očakávalo. Vplyv hypertenzie je podstatne väčší u diabetikov v porovnaní s bežnou populáciou, čo poukazuje buď na zvýšenú citlivosť k jej účinku, alebo na zavádzajúci etiopatogenetický mechanizmus hypertenzie spojený s KVCH v rámci DM2T. Tento krátky prehľad si kladie za cieľ popísať zmeny v cievnom riečisku u ľudí s diabetom v porovnaní s bežnou populáciou a skúmať hypotézy ohľadom častej príčinnosť medzi zvýšeným výskytom KVCH a hypertenzie u pacientov s diabetom.

Cardiovascular disease (CVD) is the leading cause of mortality in type 2 diabetes mellitus (T2DM), yet a significant proportion of the disease burden cannot be accounted for by conventional cardiovascular (CV) risk factors(1). Hypertension occurs in approximately 80% of people with diabetes, substantially more frequently than would be anticipated based on general population samples. Further, the impact of hypertension is substantially higher within those with diabetes than it is within the general population, suggesting either increased sensitivity to its effect or a confounding underlying aetiopathogenic mechanism of hypertension associated with CVD within diabetes. This mini-review aims to describe the changes in the vascular tree seen within people with diabetes compared to the general population and explore the hypotheses to account for the common causality of the increased prevalence of CVD and hypertension in those with diabetes.

• MeSH
• albuminurie MeSH
• ambulantní monitorování MeSH
• biologické markery MeSH
• diabetes mellitus 2. typu * komplikace   patofyziologie   MeSH
• epidemiologické studie MeSH
• hypertenze * patofyziologie   MeSH
• kardiovaskulární nemoci * etiologie   MeSH
• lidé MeSH
• mikrocirkulace * MeSH
• rasové skupiny MeSH
• rizikové faktory MeSH
• Check Tag
• lidé MeSH