Specific enhancement of sodium dependent glucose transporter 1 concentration by luminal polyamines in rat small intestine

2001 ◽  
Vol 120 (5) ◽  
pp. A677 ◽  
Author(s):  
Katsuhiro Uda ◽  
Tomoyuki Tsujikawa ◽  
Jin Satoh ◽  
Akihiko Itoh ◽  
Tetsuya Fukunaga ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Transporter ◽  
Rat Small Intestine ◽  
Glucose Transporter 1 ◽  
Specific Enhancement ◽  
Sodium Dependent

Nano chitosan–zinc complex improves the growth performance and antioxidant capacity of the small intestine in weaned piglets

2020 ◽  
pp. 1-12
Author(s):  
Minyang Zhang ◽  
Guojun Hou ◽  
Ping Hu ◽  
Dan Feng ◽  
Jing Wang ◽  
...  
Keyword(s):  
Small Intestine ◽  
Antioxidant Capacity ◽  
Growth Performance ◽  
Glucose Transporter ◽  
Zinc Complex ◽  
Weaned Piglets ◽  
Glucose Transporter 1 ◽  
Expression Levels ◽  
Weaning Stress ◽  
Related Proteins

Abstract The present study was conducted to test the hypothesis that dietary supplementation with a nano chitosan–zinc complex (CP–Zn, 100 mg/kg Zn) could alleviate weaning stress in piglets challenged with enterotoxigenic Escherichia coli K88 by improving growth performance and intestinal antioxidant capacity. The in vivo effects of CP–Zn on growth performance variables (including gastrointestinal digestion and absorption functions and the levels of key proteins related to muscle growth) and the antioxidant capacity of the small intestine (SI) were evaluated in seventy-two weaned piglets. The porcine jejunal epithelial cell line IPEC-J2 was used to further investigate the antioxidant mechanism of CP–Zn in vitro. The results showed that CP–Zn supplementation increased the jejunal villus height and decreased the diarrhoea rate in weaned piglets. CP–Zn supplementation also improved growth performance (average daily gain and average daily feed intake), increased the activity of carbohydrate digestion-related enzymes (amylase, maltase, sucrase and lactase) and the mRNA expression levels of nutrient transporters (Na+-dependent glucose transporter 1, glucose transporter type 2, peptide transporter 1 and excitatory amino acid carrier 1) in the jejunum and up-regulated the expression levels of mammalian target of rapamycin (mTOR) pathway-related proteins (insulin receptor substrate 1, phospho-mTOR and phospho-p70S6K) in muscle. In addition, CP–Zn supplementation increased glutathione content, enhanced total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-px) activity, and reduced malondialdehyde (MDA) content in the jejunum. Furthermore, CP–Zn decreased the content of MDA and reactive oxygen species, enhanced the activity of T-SOD and GSH-px and up-regulated the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway-related proteins (Nrf2, NAD(P)H:quinone oxidoreductase 1 and haeme oxygenase 1) in lipopolysaccharide-stimulated IPEC-J2 cells. Collectively, these findings indicate that CP–Zn supplementation can improve growth performance and the antioxidant capacity of the SI in piglets, thus alleviating weaning stress.

Development of sotagliflozin, a dual sodium-dependent glucose transporter 1/2 inhibitor

2015 ◽  
Vol 12 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Pablo Lapuerta ◽  
Brian Zambrowicz ◽  
Paul Strumph ◽  
Arthur Sands
Keyword(s):  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Sodium Dependent

scholarly journals Glucocorticoids Enhance Intestinal Glucose Uptake Via the Dimerized Glucocorticoid Receptor in Enterocytes

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1783-1794 ◽  
Author(s):  
Sybille D. Reichardt ◽  
Michael Föller ◽  
Rexhep Rexhepaj ◽  
Ganesh Pathare ◽  
Kerstin Minnich ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Uptake ◽  
Molecular Mechanism ◽  
Glucose Transport ◽  
Transcriptional Control ◽  
Glucose Transporter ◽  
Gene Activation ◽  
Mouse Strains ◽  
Glucose Transporter 1

Glucocorticoid (GC) treatment of inflammatory disorders, such as inflammatory bowel disease, causes deranged metabolism, in part by enhanced intestinal resorption of glucose. However, the underlying molecular mechanism is poorly understood. Hence, we investigated transcriptional control of genes reported to be involved in glucose uptake in the small intestine after GC treatment and determined effects of GC on electrogenic glucose transport from transepithelial currents. GRvillinCre mice lacking the GC receptor (GR) in enterocytes served to identify the target cell of GC treatment and the requirement of the GR itself; GRdim mice impaired in dimerization and DNA binding of the GR were used to determine the underlying molecular mechanism. Our findings revealed that oral administration of dexamethasone to wild-type mice for 3 d increased mRNA expression of serum- and GC-inducible kinase 1, sodium-coupled glucose transporter 1, and Na+/H+ exchanger 3, as well as electrogenic glucose transport in the small intestine. In contrast, GRvillinCre mice did not respond to GC treatment, neither with regard to gene activation nor to glucose transport. GRdim mice were also refractory to GC, because dexamethasone treatment failed to increase both, gene expression and electrogenic glucose transport. In addition, the rise in blood glucose levels normally observed after GC administration was attenuated in both mutant mouse strains. We conclude that enhanced glucose transport in vivo primarily depends on gene regulation by the dimerized GR in enterocytes, and that this mechanism contributes to GC-induced hyperglycemia.

Gymnemic Acids Inhibit Sodium-Dependent Glucose Transporter 1

2014 ◽  
Vol 62 (25) ◽  
pp. 5925-5931 ◽  
Author(s):  
Yu Wang ◽  
Corinna Dawid ◽  
Gabor Kottra ◽  
Hannelore Daniel ◽  
Thomas Hofmann
Keyword(s):  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Sodium Dependent

scholarly journals NHE3 Regulatory Factor 1 (NHERF1) Modulates Intestinal Sodium-dependent Phosphate Transporter (NaPi-2b) Expression in Apical Microvilli

2012 ◽  
Vol 287 (42) ◽  
pp. 35047-35056 ◽  
Author(s):  
Hector Giral ◽  
DeeAnn Cranston ◽  
Luca Lanzano ◽  
Yupanqui Caldas ◽  
Eileen Sutherland ◽  
...  
Keyword(s):  
Small Intestine ◽  
Pdz Domain ◽  
Binding Motif ◽  
Rat Small Intestine ◽  
Regulatory Factor ◽  
Sequence Analyses ◽  
C Terminus ◽  
Expression Studies ◽  
Sodium Dependent ◽  
Rat Enterocytes

Pi uptake in the small intestine occurs predominantly through the NaPi-2b (SLC34a2) co-transporter. NaPi-2b is regulated by changes in dietary Pi but the mechanisms underlying this regulation are largely undetermined. Sequence analyses show NaPi-2b has a PDZ binding motif at its C terminus. Immunofluorescence imaging shows NaPi-2b and two PDZ domain containing proteins, NHERF1 and PDZK1, are expressed in the apical microvillar domain of rat small intestine enterocytes. Co-immunoprecipitation studies in rat enterocytes show that NHERF1 associates with NaPi-2b but not PDZK1. In HEK co-expression studies, GFP-NaPi-2b co-precipitates with FLAG-NHERF1. This interaction is markedly diminished when the C-terminal four amino acids are truncated from NaPi-2b. FLIM-FRET analyses using tagged proteins in CACO-2BBE cells show a distinct phasor shift between NaPi-2b and NHERF1 but not between NaPi-2b and the PDZK1 pair. This shift demonstrates that NaPi-2b and NHERF1 reside within 10 nm of each other. NHERF1−/− mice, but not PDZK1−/− mice, had a diminished adaptation of NaPi-2b expression in response to a low Pi diet. Together these studies demonstrate that NHERF1 associates with NaPi-2b in enterocytes and regulates NaPi-2b adaptation.

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