TY  - JOUR
A1  - Jurowich, Christian Ferdinand
A1  - Otto, Christoph
A1  - Rikkala, Prashanth Reddy
A1  - Wagner, Nicole
A1  - Vrhovac, Ivana
A1  - Sabolić, Ivan
A1  - Germer, Christoph-Thomas
A1  - Koepsell, Hermann
T1  - Ileal interposition in rats with experimental type 2 like diabetes improves glycemic control independently of glucose absorption
JF  - Journal of Diabetes Research
N2  - Bariatric operations in obese patients with type 2 diabetes often improve diabetes before weight loss is observed. In patients mainly Roux-en-Y-gastric bypass with partial stomach resection is performed. Duodenojejunal bypass (DJB) and ileal interposition (IIP) are employed in animal experiments. Due to increased glucose exposition of L-cells located in distal ileum, all bariatric surgery procedures lead to higher secretion of antidiabetic glucagon like peptide-1 (GLP-1) after glucose gavage. After DJB also downregulation of Na\(^{+}\)-D-glucose cotransporter SGLT1 was observed. This suggested a direct contribution of decreased glucose absorption to the antidiabetic effect of bariatric surgery. To investigate whether glucose absorption is also decreased after IIP, we induced diabetes with decreased glucose tolerance and insulin sensitivity in male rats and investigated effects of IIP on diabetes and SGLT1. After IIP, we observed weight-independent improvement of glucose tolerance, increased insulin sensitivity, and increased plasma GLP-1 after glucose gavage. The interposed ileum was increased in diameter and showed increased length of villi, hyperplasia of the epithelial layer, and increased number of L-cells. The amount of SGLT1-mediated glucose uptake in interposed ileum was increased 2-fold reaching the same level as in jejunum. Thus, improvement of glycemic control by bariatric surgery does not require decreased glucose absorption.
KW  - glucagon like peptide-1
KW  - food intake
KW  - body weight
KW  - cotransporter SGLT1
KW  - bariatric surgery
KW  - biliopancreatic diversion
KW  - intestinal glucose
KW  - gut hormones
KW  - duodenal jejunal bypass
KW  - Y-gastric bypass
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-149166
VL  - 2015
IS  - 490365
ER  - 
TY  - JOUR
A1  - Salker, Madhuri S.
A1  - Singh, Yogesh
A1  - Zeng, Ni
A1  - Chen, Hong
A1  - Zhang, Shaqiu
A1  - Umbach, Anja T.
A1  - Fakhri, Hajar
A1  - Kohlhofer, Ursula
A1  - Quintanilla-Martinez, Leticia
A1  - Durairaj, Ruban R. Peter
A1  - Barros, Flavio S. V.
A1  - Vrljicak, Pavle
A1  - Ott, Sascha
A1  - Brucker, Sara Y.
A1  - Wallwiener, Diethelm
A1  - Madunić, Ivana Vrhovac
A1  - Breljak, Davorka
A1  - Sabolić, Ivan
A1  - Koepsell, Hermann
A1  - Brosens, Jan J.
A1  - Lang, Florian
T1  - Loss of endometrial sodium glucose cotransporter SGLT1 is detrimental to embryo survival and fetal growth in pregnancy
JF  - Scientific Reports
N2  - Embryo implantation requires a hospitable uterine environment. A key metabolic change that occurs during the peri-implantation period, and throughout early pregnancy, is the rise in endometrial glycogen content. Glycogen accumulation requires prior cellular uptake of glucose. Here we show that both human and murine endometrial epithelial cells express the high affinity Na\(^+\)-coupled glucose carrier SGLT1. Ussing chamber experiments revealed electrogenic glucose transport across the endometrium in wild type (\(Slc5a1^{+/+}\)) but not in SGLT1 defcient (\(Slc5a1^{−/−}\)) mice. Endometrial glycogen content, litter size and weight of offspring at birth were signifcantly lower in \(Slc5a1^{−/−}\) mice. In humans, \(SLC5A1\) expression was upregulated upon decidualization of primary endometrial stromal cells. Endometrial \(SLC5A1\) expression during the implantation window was attenuated in patients with recurrent pregnancy loss when compared with control subjects. Our fndings reveal a novel mechanism establishing adequate endometrial glycogen stores for pregnancy. Disruption of this histiotrophic pathway leads to adverse pregnancy outcome.
KW  - biology
KW  - embryology
KW  - intrauterine growth
KW  - paediatric research
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173814
VL  - 7
ER  -