Artocarpus lacucha Extract and Oxyresveratrol Inhibit Glucose Transporters in Human Intestinal Caco-2 Cells

Planta Medica ◽  
2021 ◽  
Author(s):  
Matusorn Wongon ◽  
Nanteetip Limpeanchob
Keyword(s):  
Glucose Transport ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Glucose Absorption ◽  
Culture Conditions ◽  
Glucose Transporter 1 ◽  
Glucose Transporter 2 ◽  
Sodium Dependent ◽  
Intestinal Glucose Absorption ◽  
Carbohydrate Digestion

AbstractReduction of intestinal glucose absorption might result from either delayed carbohydrate digestion or blockage of glucose transporters. Previously, oxyresveratrol was shown to inhibit α-glucosidase, but its effect on glucose transporters has not been explored. The present study aimed to assess oxyresveratrol-induced inhibition of the facilitative glucose transporter 2 and the active sodium-dependent glucose transporter 1. An aqueous extract of Artocarpus lacucha, Puag Haad, which is oxyresveratrol-enriched, was also investigated. Glucose transport was measured by uptake into Caco-2 cells through either glucose transporter 2 or sodium-dependent glucose transporter 1 according to the culture conditions. Oxyresveratrol (40 to 800 µM) dose-dependently reduced glucose transport, which appeared to inhibit both glucose transporter 2 and sodium-dependent glucose transporter 1. Puag Haad at similar concentrations also inhibited these transporters but with greater efficacy. Oxyresveratrol and Puag Haad could help reduce postprandial hyperglycemic peaks, which are considered to be most damaging in diabetics.

Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets

2006 ◽  
Vol 290 (2) ◽  
pp. G293-G300 ◽  
Author(s):  
J. J. Cottrell ◽  
B. Stoll ◽  
R. K. Buddington ◽  
J. E. Stephens ◽  
L. Cui ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Glucose Transporter ◽  
Glucose Absorption ◽  
Glucose Transporter 1 ◽  
Portal Vein Flow ◽  
Glucose Transporter 2 ◽  
Glucagon Like Peptide ◽  
Portal Veins

Premature infants receiving chronic total parenteral nutrition (TPN) due to feeding intolerance develop intestinal atrophy and reduced nutrient absorption. Although providing the intestinal trophic hormone glucagon-like peptide-2 (GLP-2) during chronic TPN improves intestinal growth and morphology, it is uncertain whether GLP-2 enhances absorptive function. We placed catheters in the carotid artery, jugular and portal veins, duodenum, and a portal vein flow probe in piglets before providing either enteral formula (ENT), TPN or a coinfusion of TPN plus GLP-2 for 6 days. On postoperative day 7, all piglets were fed enterally and digestive functions were evaluated in vivo using dual infusion of enteral (13C) and intravenous (2H) glucose, in vitro by measuring mucosal lactase activity and rates of apical glucose transport, and by assessing the abundances of sodium glucose transporter-1 (SGLT-1) and glucose transporter-2 (GLUT2). Both ENT and GLP-2 pigs had larger intestine weights, longer villi, and higher lactose digestive capacity and in vivo net glucose and galactose absorption compared with TPN alone. These endpoints were similar in ENT and GLP-2 pigs except for a lower intestinal weight and net glucose absorption in GLP-2 compared with ENT pigs. The enhanced hexose absorption in GLP-2 compared with TPN pigs corresponded with higher lactose digestive and apical glucose transport capacities, increased abundance of SGLT-1, but not GLUT-2, and lower intestinal metabolism of [13C]glucose to [13C]lactate. Our findings indicate that GLP-2 treatment during chronic TPN maintains intestinal structure and lactose digestive and hexose absorptive capacities, reduces intestinal hexose metabolism, and may facilitate the transition to enteral feeding in TPN-fed infants.

Functional Expression of Sodium-Dependent Glucose Transporter in Amelogenesis

2020 ◽  
Vol 99 (8) ◽  
pp. 977-986
Author(s):  
H. Ida-Yonemochi ◽  
K. Otsu ◽  
H. Harada ◽  
H. Ohshima
Keyword(s):  
Organ Culture ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Maturation Stage ◽  
Sodium Dependent ◽  
Tooth Morphogenesis

Glucose is an essential source of energy for mammalian cells and is transported into the cells by glucose transporters. There are 2 types of glucose transporters: one is a passive glucose transporter, GLUT ( SLC2A), and the other is a sodium-dependent active glucose transporter, SGLT ( SLC5A). We previously reported that the expression of GLUTs during tooth development is precisely and spatiotemporally controlled and that the glucose uptake mediated by GLUT1 plays a crucial role in early tooth morphogenesis and tooth size determination. This study aimed to clarify the localization and roles of SGLT1 and SGLT2 in murine ameloblast differentiation by using immunohistochemistry, immunoelectron microscopy, an in vitro tooth organ culture experiment, and in vivo administration of an inhibitor of SGLT1/2, phloridzin. SGLT1, which has high affinity with glucose, was immunolocalized in the early secretory ameloblasts and the ruffle-ended ameloblasts in the maturation stage. However, SGLT2, which has high glucose transport capacity, was observed in the stratum intermedium, papillary layer, and ameloblasts at the maturation stage and colocalized with Na+-K+-ATPase. The inhibition of SGLT1/2 by phloridzin in the tooth germs induced the disturbance of ameloblast differentiation and enamel matrix formation both in vitro (organ culture) and in vivo (mouse model). The expression of SGLT1 and SGLT2 was significantly upregulated in hypoxic conditions in the ameloblast-lineage cells. These findings suggest that the active glucose uptake mediated by SGLT1 and SGLT2 is strictly regulated and dependent on the intra- and extracellular microenvironments during tooth morphogenesis and that the appropriate passive and active glucose transport is an essential event in amelogenesis.

Impaired intestinal and renal glucose transport in PDK-1 hypomorphic mice

2006 ◽  
Vol 291 (5) ◽  
pp. R1533-R1538 ◽  
Author(s):  
Ferruh Artunc ◽  
Rexhep Rexhepaj ◽  
Harald Völkl ◽  
Florian Grahammer ◽  
Christine Remy ◽  
...  
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Ussing Chamber ◽  
Glucose Absorption ◽  
Renal Tubules ◽  
Glucose Transporter 1 ◽  
Glucose Reabsorption ◽  
Urinary Glucose ◽  
Proximal Tubular

The phosphoinositide-dependent kinase-1 (PDK-1) activates the serum- and glucocorticoid-inducible kinase and protein kinase B isoforms, which, in turn, are known to stimulate the renal and intestinal Na+-dependent glucose transporter 1. The present study has been performed to explore the role of PDK-1 in electrogenic glucose transport in small intestine and proximal renal tubules. To this end, mice expressing ∼20% of PDK-1 ( pdk1 hm) were compared with their wild-type littermates ( pdk1 wt). According to Ussing chamber experiments, electrogenic glucose transport was significantly smaller in the jejunum of pdk1 hm than of pdk1 wt mice. Similarly, proximal tubular electrogenic glucose transport in isolated, perfused renal tubule segments was decreased in pdk1 hm compared with pdk1 wt mice. Intraperitoneal injection of 3 g/kg body wt glucose resulted in a similar increase of plasma glucose concentration in pdk1 hm and in pdk1 wt mice but led to a higher increase of urinary glucose excretion in pdk1 hm mice. In conclusion, reduction of functional PDK-1 leads to impairment of electrogenic intestinal glucose absorption and renal glucose reabsorption. The experiments disclose a novel element of glucose transport regulation in kidney and small intestine.

Inhibition of the intestinal postprandial glucose transport by gallic acid and gallic acid derivatives

2021 ◽  
Author(s):  
huijun Wang ◽  
Mark I Fowler ◽  
David J Messenger ◽  
Jose Juan Ordaz-Ortiz ◽  
Xuelan Gu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gallic Acid ◽  
Glucose Transporter ◽  
Postprandial Glucose ◽  
Postprandial Blood Glucose ◽  
Glucose Transporter 1 ◽  
Glucose Levels ◽  
Glucose Transporter 2 ◽  
Blood Glucose Levels ◽  
Sodium Dependent

Inhibition of glucose uptake in the intestine through sodium-dependent glucose transporter 1 (SGLT1) or glucose transporter 2 (GLUT2) may be beneficial in controlling postprandial blood glucose levels. Gallic acid and...

Selective sodium-dependent glucose transporter 1 inhibitors block glucose absorption and impair glucose-dependent insulinotropic peptide release

2015 ◽  
Vol 308 (11) ◽  
pp. G946-G954 ◽  
Author(s):  
Robert L. Dobbins ◽  
Frank L. Greenway ◽  
Lihong Chen ◽  
Yaping Liu ◽  
Sharon L. Breed ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Peptide Yy ◽  
Human Subjects ◽  
Glucose Absorption ◽  
Fecal Excretion ◽  
Cell Secretion ◽  
Inhibitory Peptide ◽  
Healthy Human ◽  
Glucose Transporter 1 ◽  
Sodium Dependent

GSK-1614235 and KGA-2727 are potent, selective inhibitors of the SGLT1 sodium-dependent glucose transporter. Nonclinical (KGA-2727) and clinical (GSK-1614235) trials assessed translation of SGLT1 inhibitor effects from rats to normal human physiology. In rats, KGA-2727 (0.1 mg/kg) or vehicle was given before oral administration of 3- O-methyl-α-d-glucopyranose (3- O-methylglucose, 3-OMG) containing 3-[3H]OMG tracer. Tracer absorption and distribution were assessed from plasma, urine, and fecal samples. SGLT1 inhibition reduced urine 3-OMG recovery and increased fecal excretion. SGLT1 inhibitor effects on plasma glucose, insulin, gastric inhibitory peptide (GIP), and glucagon-like peptide-1 (GLP-1) concentrations were also measured during a standard meal. Incremental glucose, insulin, and GIP concentrations were decreased, indicating downregulation of β-cell and K cell secretion. Minimal effects were observed in the secretion of the L cell product, GLP-1. With the use of a three-way, crossover design, 12 healthy human subjects received placebo or 20 mg GSK-1614235 immediately before or after a meal. Five minutes into the meal, 3-OMG was ingested. Postmeal dosing had little impact, yet premeal dosing delayed and reduced 3-OMG absorption, with an AUC0–10 of 231 ± 31 vs. 446 ± 31 μg·h−1·ml−1, for placebo. Recovery of tracer in urine was 1.2 ± 0.7 g for premeal dosing and 2.2 ± 0.1 g for placebo. Incremental concentrations of insulin, C-peptide, and GIP were reduced for 2 h with premeal GSK-1614235. Total GLP-1 concentrations were significantly increased, and a trend for increased peptide YY (PYY) was noted. SGLT1 inhibitors block intestinal glucose absorption and reduce GIP secretion in rats and humans, suggesting SGLT1 glucose transport is critical for GIP release. Conversely, GLP-1 and PYY secretion are enhanced by SGLT1 inhibition in humans.

scholarly journals Estriol blunts postprandial blood glucose rise in male rats through regulating intestinal glucose transporters

2015 ◽  
Vol 308 (5) ◽  
pp. E370-E379 ◽  
Author(s):  
Noriko Yamabe ◽  
Ki Sung Kang ◽  
Woojung Lee ◽  
Su-Nam Kim ◽  
Bao Ting Zhu
Keyword(s):  
Blood Glucose ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Male Rats ◽  
Postprandial Blood Glucose ◽  
Oral Glucose ◽  
Glucose Transporter 1 ◽  
Glucose Transporter 2 ◽  
17Β Estradiol

Despite increased total food intake in healthy, late-stage pregnant women, their peak postprandial blood sugar levels are normally much lower than the levels seen in healthy nonpregnant women. In this study, we sought to determine whether estriol (E3), an endogenous estrogen predominantly produced during human pregnancy, contributes to the regulation of the postprandial blood glucose level in healthy normal rats. In vivo studies using rats showed that E3 blunted the speed and magnitude of the blood glucose rise following oral glucose administration, but it did not appear to affect the total amount of glucose absorbed. E3 also did not affect insulin secretion, but it significantly reduced the rate of intestinal glucose transport compared with vehicle-treated animals. Consistent with this finding, expression of the sodium-dependent glucose transporter 1 and 2 was significantly downregulated by E3 treatment in the brush-border membrane and basolateral membrane, respectively, of enterocytes. Most of the observed in vivo effects were noticeably stronger with E3 than with 17β-estradiol. Using differentiated human Caco-2 enterocyte monolayer culture as an in vitro model, we confirmed that E3 at physiologically relevant concentrations could directly inhibit glucose uptake via suppression of glucose transporter 2 expression, whereas 17β-estradiol did not have a similar effect. Collectively, these data showed that E3 can blunt the postprandial glycemic surge in rats through modulating the level of intestinal glucose transporters.

scholarly journals The Role of Sodium-Dependent Glucose Transporter 1 and Glucose Transporter 2 in the Absorption of Cyanidin-3-O-β-Glucoside in Caco-2 Cells

Nutrients ◽  
2014 ◽  
Vol 6 (10) ◽  
pp. 4165-4177 ◽  
Author(s):  
Tang-Bin Zou ◽  
Dan Feng ◽  
Gang Song ◽  
Hua-Wen Li ◽  
Huan-Wen Tang ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Glucose Transporter 2 ◽  
Sodium Dependent

Heat stress increases apical glucose transport in the chicken jejunum

2006 ◽  
Vol 290 (1) ◽  
pp. R195-R201 ◽  
Author(s):  
Carles Garriga ◽  
Richard R. Hunter ◽  
Concepció Amat ◽  
Joana M. Planas ◽  
Malcolm A. Mitchell ◽  
...  
Keyword(s):  
Heat Stress ◽  
Food Intake ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Body Weight Gain ◽  
Intestinal Adaptation ◽  
Sugar Uptake ◽  
Glucose Transporter 1 ◽  
Glucose Transporter 2 ◽  
Ad Libitum

In chickens, elevated environmental temperature reduces food intake. We have previously reported that, during heat stress, the intestinal mucosa has an increased capacity to take up sugars. To investigate whether the effects of warm environment on sugar uptake are an intestinal adaptation to lower energy intake or a response attributable to heat stress, we examined the glucose transport kinetics of apical and basolateral membranes of the jejunum and the mucosal morphology of broiler chickens maintained in climatic chambers for 2 wk. Experimental groups were 1) control ad libitum (CAL), fed ad libitum and in thermoneutral conditions (20°C); 2) heat stress ad libitum (HSAL), fed ad libitum and kept in a heated environment (30°C); and 3) control pair-fed (CPF), maintained in thermoneutral conditions and fed the same amount of food as that consumed by the HSAL group. Both the CPF and the HSAL groups showed reduced body weight gain, but only the HSAL chickens had lower plasma thyroid hormones and higher corticosterone than CAL and CPF groups. The fresh weight and length of the jejunum were only reduced in the HSAL group. The activity and expression of apical sodium-dependent glucose transporter 1 (SGLT-1) were increased by ∼50% in the HSAL chickens, without effects in the CPF group. No changes in Kd or in SGLT-1 and glucose transporter-2 Km were observed in the pair-fed and heated birds. These results support the view that increased intestinal hexose transport capacity is entirely dependent on adaptations of apical SGLT-1 expression to heat stress and is not due to reduced food intake.

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