Dietary Fructose Inhibits Intestinal Calcium Absorption and Induces Vitamin D Insufficiency in CKD

Douard, Véronique; Asgerally, Abbas; Sabbagh, Yves; Sugiura, Shozo; Shapses, Sue A.; Casirola, D.; Ferraris, Ronaldo P.

doi:10.1681/asn.2009080795

Cited by 43 publications

(72 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We previously showed that active, diet-inducible Ca 2ϩ transport parallels this marked proximal to distal gradient in Ca 2ϩ transporter expression (21,25 transport clearly is not affected by fructose metabolism and acute fructose-induced reductions in ATP concentrations because 1) transcellular Ca 2ϩ transport remains unchanged with or without supplementation with glutamine, a major source of respiratory fuel and metabolic energy for intestinal cells (17,58,74), and 2) Ca 2ϩ transport is greater in fructose-compared with glucose-incubated sacs from KHK Ϫ/Ϫ and GLUT5…”

Section: Discussionmentioning

confidence: 86%

“…Chronic vs. acute effects of sugars on intestinal Ca 2ϩ transport. We previously showed that, in rats and mice with high Ca 2ϩ requirements (e.g., during lactation) or that are nutritionally deficient in Ca 2ϩ , compensatory increases in 1,25-(OH) 2 D 3 -regulated intestinal Ca 2ϩ absorption is strongly inhibited by chronic consumption of dietary fructose (21,24,25). The mechanism underlying this chronic fructose effect is a fructose-induced decrease in levels of 1␣-hydroxylase, the enzyme synthesizing 1,25-(OH) 2 D 3 .…”

Section: Discussionmentioning

confidence: 99%

“…Real-time PCR was performed using Mx3000P (Stratagene Real-Time PCR System, La Jolla, CA), as described previously (21). Primers were designed using Roche primer design software (http://www.roche-applied-science.com) and were purchased from Integrated DNA Technologies (IDT, Coralville, IA) ( Table 1).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Acute interactions between intestinal sugar and calcium transport in vitro

Tharabenjasin

Douard

Patel

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

Fructose consumption by Americans has increased markedly, whereas Ca2+ intake has decreased below recommended levels. Because fructose metabolism decreases enterocyte ATP concentrations, we tested the hypothesis that luminal fructose acutely reduces active, diet-inducible Ca2+ transport in the small intestine. We confirmed that the decrease in ATP concentrations was indeed greater in fructose- compared with glucose-incubated mucosal homogenates from wild-type and was prevented in fructose-incubated homogenates from ketohexokinase (KHK)−/− mice. We then induced active Ca2+ transport by chronically feeding wild-type, fructose transporter glucose transporter 5 (GLUT5)−/−, as well as KHK−/− mice a low Ca2+ diet and measured transepithelial Ca2+ transport in everted duodenal sacs incubated in solutions containing glucose, fructose, or their nonmetabolizable analogs. The diet-induced increase in active Ca2+ transport was proportional to dramatic increases in expression of the Ca2+-selective channel transient receptor potential vanilloid family calcium channel 6 as well as of the Ca2+-binding protein 9k (CaBP9k) but not that of the voltage-dependent L-type channel Ca(v)1.3. Crypt-villus distribution of CaBP9k seems heterogeneous, but low Ca2+ diets induce expression in more cells. In contrast, KHK distribution is homogeneous, suggesting that fructose metabolism can occur in all enterocytes. Diet-induced Ca2+ transport was not enhanced by addition of the enterocyte fuel glutamine and was always greater in sacs of wild-type, GLUT5−/−, and KHK−/− mice incubated with fructose or nonmetabolizable sugars than those incubated with glucose. Thus duodenal Ca2+ transport is not affected by fructose and enterocyte ATP concentrations but instead may decrease with glucose metabolism, as Ca2+ transport remains high with 3- O-methylglucose that is also transported by sodium-glucose cotransporter 1 but cannot be metabolized.

show abstract

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Acute interactions between intestinal sugar and calcium transport in vitro

Tharabenjasin

Douard

Patel

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

show abstract

“…Intestinal uptake rates were determined as described previously (45,46). Briefly, 1-cm segments of the proximal small intestine were individually mounted and everted on grooved steel rods.…”

Section: Methodsmentioning

confidence: 99%

Cdc42 and Rab8a are critical for intestinal stem cell division, survival, and differentiation in mice

Sakamori¹,

Das²,

Yu³

et al. 2012

J. Clin. Invest.

Self Cite

121

View full text Add to dashboard Cite

The constant self renewal and differentiation of adult intestinal stem cells maintains a functional intestinal mucosa for a lifetime. However, the molecular mechanisms that regulate intestinal stem cell division and epithelial homeostasis are largely undefined. We report here that the small GTPases Cdc42 and Rab8a are critical regulators of these processes in mice. Conditional ablation of Cdc42 in the mouse intestinal epithelium resulted in the formation of large intracellular vacuolar structures containing microvilli (microvillus inclusion bodies) in epithelial enterocytes, a phenotype reminiscent of human microvillus inclusion disease (MVID), a devastating congenital intestinal disorder that results in severe nutrient deprivation. Further analysis revealed that Cdc42-deficient stem cells had cell division defects, reduced capacity for clonal expansion and differentiation into Paneth cells, and increased apoptosis. Cdc42 deficiency impaired Rab8a activation and its association with multiple effectors, and prevented trafficking of Rab8a vesicles to the midbody. This impeded cytokinesis, triggering crypt apoptosis and disrupting epithelial morphogenesis. Rab8a was also required for Cdc42-GTP activity in the intestinal epithelium, where continued cell division takes place. Furthermore, mice haploinsufficient for both Cdc42 and Rab8a in the intestine demonstrated abnormal crypt morphogenesis and epithelial transporter physiology, further supporting their functional interaction. These data suggest that defects of the stem cell niche can cause MVID. This hypothesis represents a conceptual departure from the conventional view of this disease, which has focused on the affected enterocytes, and suggests stem cell-based approaches could be beneficial to infants with this often lethal condition.

show abstract

“…Therefore, it is an important analyte in the food industry. However, excessive and prolonged consumption of Dfructose may lead to the development of metabolic disorders: renal and non-alcoholic fatty liver diseases, metabolic syndrome, obesity, diabetes and others [2][3][4][5]. Thus, this metabolite is also relevant for clinical diagnostics and has to be controlled in daily intake.…”

Section: Introductionmentioning

confidence: 99%