Urinary Chiro- and Myo-Inositol Levels as a Biological Marker for Type 2 Diabetes Mellitus

Hong, Jun Hwa; Jang, Hye Won; Kang, Yea Eun; Lee, Ju Hee; Kim, Koon Soon; Kim, Hyun Jin; Park, Kyu Ri; Ku, Bon Jeong

doi:10.1155/2012/734718

Cited by 25 publications

(22 citation statements)

References 22 publications

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“…However, in both type-1 and type-2 diabetes mellitus their urinary excretion are markedly elevated, a phenomenon known as inosituria. 5,7,8 This abnormal inositol excretion is also associated with a selective 4-to 7-fold increase in DCI urinary excretion compared to MI, which is inversely correlated with measures of insulin sensitivity. 5,7 The multiplied product of DCI and MI urinary concentrations has even been suggested to have potential utility as a predictive biomarker for type-2 diabetes mellitus in humans.…”

Section: Introductionmentioning

confidence: 91%

The diabetic rat kidney mediates inosituria and selective urinary partitioning of D-chiro-inositol

Chang

Choong

Phillips

et al. 2014

Exp Biol Med (Maywood)

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Diabetic nephropathy is a serious complication of diabetes mellitus with a pressing need for effective metabolic markers to detect renal impairment. Of potential significance are the inositol compounds, myo-inositol (MI), and the less abundant stereoisomer, D-chiro-inositol (DCI), which are excreted at increased levels in the urine in diabetes mellitus, a phenomenon known as inosituria. There is also a selective urinary excretion of DCI compared to MI. As the biological origins of altered inositol metabolism in diabetes mellitus are unknown, the aim of this study was to determine whether the diabetic kidney was directly responsible. Kidneys isolated from four-week streptozotocin-induced diabetic rats were characterized by a 3-fold reduction in glomerular filtration rate (GFR) compared to matched non-diabetic kidneys. When perfused with fixed quantities of MI (50 mM) and DCI (5 mM) under normoglycemic conditions (5 mM glucose), GFR-normalized urinary excretion of MI was increased by 1.7-fold in diabetic vs. non-diabetic kidneys. By comparison, GFR-normalized urinary excretion of DCI was increased by 4-fold. Perfusion conditions replicating hyperglycemia (20 mM glucose) potentiated DCI but not MI urinary excretion in both non-diabetic and diabetic kidneys. Overall, there was a 2.4-fold increase in DCI urinary excretion compared to MI in diabetic kidneys that was independent of glucose ambience. This increased urinary excretion of DCI and MI in diabetic kidneys occurred despite increased renal expression of the inositol transporters, sodium myo-inositol transporter subtype 1 and 2 (SMIT1 and SMIT2). These findings show that the diabetic kidney primarily mediates inosituria and altered urinary partitioning of MI and DCI. Urinary inositol levels might therefore serve as an indicator of impaired renal function in diabetes mellitus with wider implications for monitoring chronic kidney disease.

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Section: Introductionmentioning

confidence: 91%

The diabetic rat kidney mediates inosituria and selective urinary partitioning of D-chiro-inositol

Chang

Choong

Phillips

et al. 2014

Exp Biol Med (Maywood)

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“…Inositol is an important constituent of living cells that is known to take part in various cellular processes, including the development of peripheral nerves (2) and osteogenesis (3). Abnormal inositol metabolism has been reported in both type 1 and type 2 diabetes, as reflected by elevated urinary MI and D-chiro-inositol excretion (4)(5)(6). Indeed, MI supplementation has been documented to prevent the onset of gestational diabetes (7)(8)(9).…”

mentioning

confidence: 99%

Identification and Functional Implications of Sodium/Myo-Inositol Cotransporter 1 in Pancreatic β-Cells and Type 2 Diabetes

Cheng

Zhang

et al. 2017

Diabetes

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-inositol (MI), the precursor of the second messenger phosphoinositide (PI), mediates multiple cellular events. Rat islets exhibit active transport of MI, although the mechanism involved remains elusive. Here, we report, for the first time, the expression of sodium/-inositol cotransporter 1 (SMIT1) in rat islets and, specifically, β-cells. Genetic or pharmacological inhibition of SMIT1 impaired glucose-stimulated insulin secretion by INS-1E cells, probably via downregulation of PI signaling. In addition, SMIT1 expression in INS-1E cells and isolated islets was augmented by acute high-glucose exposure and reduced in chronic hyperglycemia conditions. In corroboration, chronic MI treatment improved the disease phenotypes of diabetic rats and islets. On the basis of our results, we postulate that the MI transporter SMIT1 is required to maintain a stable PI pool in β-cells in order that PI remains available despite its rapid turnover.

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“…Under normal conditions, up to 98% of myo-inositol is reabsorbed in the renal tubules. Consequently, increased concentrations of myo-inositol could be considered as an indication of ongoing pathological changes in the renal system: increased concentrations of urinary myo-inositol were reported for patients with diabetes and renal failure [26][27][28] . For our case myo-inositol is interesting because its alteration during recovery from UTI would eventually be related not to the bacterial metabolism but to the renal function.…”

Section: Resultsmentioning

confidence: 99%

Exploratory analysis of urinary tract infection using a GC-APCI-MS platform

Pacchiarotta

Derks

Nevedomskaya

et al. 2015

Analyst

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Urinary tract infection (UTI) is among the most common bacterial infections worldwide. The understanding of the physiological mechanisms affected by UTI may need modern integrative '-omics' technologies, and metabolomics in particular. Here we present the first GC-APCI-MS-based explorative metabolomics study of UTI, using MS and FID detectors simultaneously. This provides high quality mass spectral data as well as semi-quantitative information demonstrating the feasibility of the GC-APCI-MS platform for non-targeted approaches. The work is part of a bigger project aiming at providing a comprehensive overview of UTI-induced changes in urine. Taking advantage of a fully clinically characterized cohort that offers the possibility of both case-control and longitudinal modelling, we can define UTI-induced change as a list of urinary metabolites which distinguish E. coli UTI patients from the subjects with no signs of an active infection. The list of molecular descriptors includes compounds related to bacterial activity such as lactic acid and lactose while other molecules show an association with the physiological status (inositol, citric acid).

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Urinary Chiro- and Myo-Inositol Levels as a Biological Marker for Type 2 Diabetes Mellitus

Cited by 25 publications

References 22 publications

The diabetic rat kidney mediates inosituria and selective urinary partitioning of D-chiro-inositol

The diabetic rat kidney mediates inosituria and selective urinary partitioning of D-chiro-inositol

Identification and Functional Implications of Sodium/Myo-Inositol Cotransporter 1 in Pancreatic β-Cells and Type 2 Diabetes

Exploratory analysis of urinary tract infection using a GC-APCI-MS platform

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