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The role of salt in the pathogenesis of fructose-induced hypertension.

Soleimani M, Alborzi P - Int J Nephrol (2011)

Bottom Line: Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension.These studies point to a novel interaction between the fructose-absorbing transporter, Glut5, and the salt transporters, NHE3 and PAT1, in the intestine and kidney proximal tubule.This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload.

View Article: PubMed Central - PubMed

Affiliation: The Center on Genetics of Transport and Epithelial Biology, University of Cincinnati, 231 Albert Sabin Way, MSB 6312, Cincinnati, OH 45267-0585, USA.

ABSTRACT
Metabolic syndrome, as manifested by visceral obesity, hypertension, insulin resistance, and dyslipidemia, is reaching epidemic proportions in the Western World, specifically the United States. Epidemiologic studies suggest that the increased prevalence of metabolic syndrome directly correlates with an increase in the consumption of fructose, mainly in the form of high-fructose corn syrup. This inexpensive alternative to traditional sugar has been increasingly utilized by the food industry as a sweetener since the 1960s. While augmented caloric intake and sedentary lifestyles play important roles in the increasing prevalence of obesity, the pathogenesis of hypertension in metabolic syndrome remains controversial. One intriguing observation points to the role of salt in fructose-induced hypertension. Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension. These studies point to a novel interaction between the fructose-absorbing transporter, Glut5, and the salt transporters, NHE3 and PAT1, in the intestine and kidney proximal tubule. This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload.

No MeSH data available.


Related in: MedlinePlus

Localization of Glut2 and Glut5 in jejunum and their regulation in response to increased dietary fructose intake. Glut5 which only transports fructose but not glucose resides in the apical membrane at basal state (a) and is activated in response to increased dietary fructose intake (b). Glut2 which can transport both glucose and fructose is expressed in the cytoplasm and on basolateral membrane at basal state (a) and is recruited to the apical membrane in the presence of increased dietary fructose or glucose intake.
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Related In: Results  -  Collection


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fig1: Localization of Glut2 and Glut5 in jejunum and their regulation in response to increased dietary fructose intake. Glut5 which only transports fructose but not glucose resides in the apical membrane at basal state (a) and is activated in response to increased dietary fructose intake (b). Glut2 which can transport both glucose and fructose is expressed in the cytoplasm and on basolateral membrane at basal state (a) and is recruited to the apical membrane in the presence of increased dietary fructose or glucose intake.

Mentions: Fructose is absorbed in the small intestine and kidney proximal tubule, predominantly via Glut5 and Glut2, which are members of facilitative carbohydrate transporting family [36–41]. Glut5 is exclusively transporting fructose while Glut2 is capable of transporting both glucose and fructose [36–41]. Glut5 is expressed on the apical membrane of enterocytes; whereas, Glut2 is located intracellularly and on the basolateral membrane at basal state. Both Glut5 and Glut2 are upregulated in response to high levels of dietary fructose intake; however, in the presence of elevated fructose or glucose intake it is Glut2 that is recruited from the basolateral to the apical membrane while Glut5 remains in its original apical position [39–41]. Figures 1(a) and 1(b) depicts the localization and role of Glut2 and Glut5 in fructose absorption in jejunum at basal state (a) and in response to increased dietary fructose intake (b).


The role of salt in the pathogenesis of fructose-induced hypertension.

Soleimani M, Alborzi P - Int J Nephrol (2011)

Localization of Glut2 and Glut5 in jejunum and their regulation in response to increased dietary fructose intake. Glut5 which only transports fructose but not glucose resides in the apical membrane at basal state (a) and is activated in response to increased dietary fructose intake (b). Glut2 which can transport both glucose and fructose is expressed in the cytoplasm and on basolateral membrane at basal state (a) and is recruited to the apical membrane in the presence of increased dietary fructose or glucose intake.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3140039&req=5

fig1: Localization of Glut2 and Glut5 in jejunum and their regulation in response to increased dietary fructose intake. Glut5 which only transports fructose but not glucose resides in the apical membrane at basal state (a) and is activated in response to increased dietary fructose intake (b). Glut2 which can transport both glucose and fructose is expressed in the cytoplasm and on basolateral membrane at basal state (a) and is recruited to the apical membrane in the presence of increased dietary fructose or glucose intake.
Mentions: Fructose is absorbed in the small intestine and kidney proximal tubule, predominantly via Glut5 and Glut2, which are members of facilitative carbohydrate transporting family [36–41]. Glut5 is exclusively transporting fructose while Glut2 is capable of transporting both glucose and fructose [36–41]. Glut5 is expressed on the apical membrane of enterocytes; whereas, Glut2 is located intracellularly and on the basolateral membrane at basal state. Both Glut5 and Glut2 are upregulated in response to high levels of dietary fructose intake; however, in the presence of elevated fructose or glucose intake it is Glut2 that is recruited from the basolateral to the apical membrane while Glut5 remains in its original apical position [39–41]. Figures 1(a) and 1(b) depicts the localization and role of Glut2 and Glut5 in fructose absorption in jejunum at basal state (a) and in response to increased dietary fructose intake (b).

Bottom Line: Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension.These studies point to a novel interaction between the fructose-absorbing transporter, Glut5, and the salt transporters, NHE3 and PAT1, in the intestine and kidney proximal tubule.This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload.

View Article: PubMed Central - PubMed

Affiliation: The Center on Genetics of Transport and Epithelial Biology, University of Cincinnati, 231 Albert Sabin Way, MSB 6312, Cincinnati, OH 45267-0585, USA.

ABSTRACT
Metabolic syndrome, as manifested by visceral obesity, hypertension, insulin resistance, and dyslipidemia, is reaching epidemic proportions in the Western World, specifically the United States. Epidemiologic studies suggest that the increased prevalence of metabolic syndrome directly correlates with an increase in the consumption of fructose, mainly in the form of high-fructose corn syrup. This inexpensive alternative to traditional sugar has been increasingly utilized by the food industry as a sweetener since the 1960s. While augmented caloric intake and sedentary lifestyles play important roles in the increasing prevalence of obesity, the pathogenesis of hypertension in metabolic syndrome remains controversial. One intriguing observation points to the role of salt in fructose-induced hypertension. Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension. These studies point to a novel interaction between the fructose-absorbing transporter, Glut5, and the salt transporters, NHE3 and PAT1, in the intestine and kidney proximal tubule. This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload.

No MeSH data available.


Related in: MedlinePlus