Regulation of SGLT1 expression in response to Na<sup>+</sup>  intake

Barfull, A.; Garriga, Carles; Tauler, Albert; Planas, Joana M.

doi:10.1152/ajpregu.00263.2001

Cited by 18 publications

(10 citation statements)

References 27 publications

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“…(3) disappeared after either inhibition of ANG II synthesis or ANG II type 1 receptor (AT1) blockade. In addition, aldosterone regulates the expression of SGLT1 in the chicken intestine under low-sodium intake posttranscriptionally (2,22). In the present study, although we have not measured ANG levels, we have found an increase in the aldosterone levels in SHR when compared with WKY rats, which could be related with the observed changes in SGLT1 function and expression in the intestine of these rats.…”

Section: Discussioncontrasting

confidence: 56%

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Mate¹,

Barfull²,

Hermosa³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Experimental models of hypertension, such as spontaneously hypertensive rats (SHR), show alterations in cellular sodium transport that affects Na(+)-coupled cotransport processes and has been involved in the pathogenesis of this disease. The objective of the present study was to analyze the kinetic properties of the sodium-dependent glucose transport in the jejunum and ileum of SHR and its genetic control, Wistar-Kyoto (WKY) rats, as well as the regulation of the transporter, SGLT1. In hypertensive rats, the increased systolic blood pressure was accompanied by an enhancement of serum aldosterone levels compared with WKY rats, but no alterations were found in their body weight or serum glucose/insulin levels. The values for d-glucose maximal rate of transport (V(max)) were 42 and 60% lower, respectively, in the jejunum and ileum of SHR than those from WKY rats. On the other hand, the values for the Michaelis constant (K(m)) were similar in both animal groups, as was the diffusive component of transport (K(d)). Immunoblotting and Northern blot analysis revealed the existence of a lower abundance of SGLT1 protein and mRNA in SHR. Moreover, hypertensive rats showed a decrease in the molecular mass of SGLT1 that could not be explained in terms of different glycosylation and/or phosphorylation levels or an alternative splicing in the expression of the protein. These findings demonstrate that SGLT1 is regulated at a transcriptional level in the intestine of hypertensive rats, and suggest that this transporter might participate in the dysregulation of sodium transport observed in hypertension.

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Section: Discussioncontrasting

confidence: 56%

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Mate¹,

Barfull²,

Hermosa³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Kojima et al (1999) also showed an increased expression of SGLT1 mRNA in the initial portion of jejunum in rats. However, Barfull et al (2002) did not find local differences in SGLT1 mRNA expression along the intestine of chickens. As the presence of SGLT1 mRNA alone did not establish the presence of the protein; western blotting and uptake studies were done to confirm that SGLT1 had a functional role along the small intestine.…”

Section: Discussionmentioning

confidence: 67%

Influence of starch and casein administered postruminally on small intestinal sodium-glucose cotransport activity and expression

Guimarães

Hazelton

Matthews

et al. 2007

Braz. arch. biol. technol.

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Twenty-four Holstein steer calves (88 ± 3kg) with abomasal catheters were randomly assigned within blocks to one of four treatments. The treatments consisted of four abomasal infusions: water (control), 4 g/kg BW.d-1 of partially hydrolyzed starch (SH), 0.6 g/kg BW.d-1 of casein, and a mix of SH + casein. The small intestine was collected and five equidistan, 1m sites were identified (duodenum, jejunum 1, jejunum 2 jejunum 3 and ileum). Maltase specific activity in mucosal homogenate and brush border membrane vesicles, SGLT1 protein abundance, and sodium-dependent glucose uptake in brush border membrane vesicles did not differ between the calves receiving different abomasal infusion treatments. However, maltase specific activity in homogenates and brush border membrane vesicles increased four-fold from the duodenum to the first jejunal site before declining steadily towards the ileum (p=0.0145 p=0.0020, respectively). The SGLT1 abundance differed by intestinal sampling site (p=0.0162). These data indicated that cattle might not have the ability to alter the capacity for glucose uptake when challenged with different substrates and that the regulation of SGLT1 expression could differ between bovine and other species

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“…For example, a high glucose diet and high sodium diet can increase the expression of intestinal SGLT1 on the transcriptional level [60, 61, 63]. The sweet taste receptor subunit T1R3 and the taste G protein gustducin, expressed in enteroendocrine L-cells, are involved in intestinal sensing of dietary sugar and artificial sweeteners which subsequently up-regulates intestinal SGLT1 mRNA and protein expression [64, 65].…”

Section: Luminal Nutrients Upregulate Intestinal Sglt1 Expressionmentioning

confidence: 99%

Sodium glucose cotransporter SGLT1 as a therapeutic target in diabetes mellitus

Song

Ōnishi

Koepsell

et al. 2016

Expert Opinion on Therapeutic Targets

143

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Introduction Glycemic control is important in diabetes mellitus to minimize the progression of the disease and the risk of potentially devastating complications. Inhibition of the sodium–glucose cotransporter SGLT2 induces glucosuria and has been established as a new anti-hyperglycemic strategy. SGLT1 plays a distinct and complementing role to SGLT2 in glucose homeostasis and, therefore, SGLT1 inhibition may also have therapeutic potential. Areas covered This review focuses on the physiology of SGLT1 in the small intestine and kidney and its pathophysiological role in diabetes. The therapeutic potential of SGLT1 inhibition, alone as well as in combination with SGLT2 inhibition, for anti-hyperglycemic therapy are discussed. Additionally, this review considers the effects on other SGLT1-expressing organs like the heart. Expert opinion SGLT1 inhibition improves glucose homeostasis by reducing dietary glucose absorption in the intestine and by increasing the release of gastrointestinal incretins like glucagon-like peptide-1. SGLT1 inhibition has a small glucosuric effect in the normal kidney and this effect is increased in diabetes and during inhibition of SGLT2, which deliver more glucose to SGLT1 in late proximal tubule. In short-term studies, inhibition of SGLT1 and combined SGLT1/SGLT2 inhibition appeared to be safe. More data is needed on long-term safety and cardiovascular consequences of SGLT1 inhibition.

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Regulation of SGLT1 expression in response to Na⁺ intake

Cited by 18 publications

References 27 publications

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Influence of starch and casein administered postruminally on small intestinal sodium-glucose cotransport activity and expression

Sodium glucose cotransporter SGLT1 as a therapeutic target in diabetes mellitus

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Regulation of SGLT1 expression in response to Na+ intake

Cited by 18 publications

References 27 publications

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Regulation of sodium-glucose cotransporter SGLT1 in the intestine of hypertensive rats

Influence of starch and casein administered postruminally on small intestinal sodium-glucose cotransport activity and expression

Sodium glucose cotransporter SGLT1 as a therapeutic target in diabetes mellitus

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Regulation of SGLT1 expression in response to Na⁺ intake