Determination of Urinary<i>Myo</i>-/<i>Chiro</i>-Inositol Ratios from Korean Diabetes Patients

Jung, Tae Sik; Hahm, Jong Ryeal; Kim, Jong-Jin; Jung, Jung-Hwa; Kang, Mi-Yeon; Moon, Sungwon; Lee, Kang-Wan; Kim, Ho-Cheol; Lee, Jong-Deog; Kim, Jihye; Kim, Deok Ryong; Chung, Se-Kyo

doi:10.3349/ymj.2005.46.4.532

Cited by 15 publications

(13 citation statements)

References 21 publications

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“…In an independent study, urine ratios of myo-inositol/chiro-inositol in control subjects were ~3 compared with 10 in type I diabetic patients and ~20 in type II diabetic patients (53). In a review of the published literature, we reported increased ratios of urine myo-inositol to chiro-inositol in our data, data from a Japanese study and data from separate investigators in the US (52).…”

Section: R E V I E W a R T I C L E M O L M Esupporting

confidence: 53%

D-Chiro-Inositol Glycans in Insulin Signaling and Insulin Resistance

Larner

Brautigan

Thorner

2010

Mol Med

158

156

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SYNTHESISInsulin stimulates both glucose transport and glycogen synthesis; however, these actions sometimes occur in a disconnected manner. Current models for the mechanism of action for insulin, for which the dominant paradigm involves the activity of the insulin receptor Tyr kinase and its primary Tyr phosphorylated substrates-the insulin receptor substrate (IRS) family of proteins (1), are inadequate to account for these historical observations. Under certain conditions, control of glucose transport by insulin is observed in the absence of an effect on glycogen synthesis, whereas under other conditions, control of glycogen synthesis by insulin is observed in the absence of an effect on glucose transport. For example, application of insulin during perfusion of the rat heart stimulated glucose transport, but did not activate glycogen synthase (GS) (2). On the other hand, when the rat diaphragm was treated with N-ethylmaleimide, to test the effect of this sulfhydryl reagent on metabolism, no effect of insulin was observed on glucose transport, but insulin-activated GS and glycogen synthesis (3). Thus, insulin signaling proceeded along one pathway while another pathway was unaffected, suggesting the possibility that no single pathway accounts for events downstream of the IR, but parallel signaling connects the IR to activation of glucose transport and glucose metabolism. These considerations led us to the concept that a cytoplasmic second messenger was generated in parallel with the phosphorylation events initiated by the receptor Tyr kinase (4). We have emphasized the hypothesis that the phosphorylation network and the second messenger pathway operate in parallel and together are required to fully account for insulin effects on metabolic disposal of intracellular glucose (4). EVIDENCE FOR INSULIN SECOND MESSENGERSThe initial evidence to support the existence of a second messenger for insulin followed classical methods used to discover cAMP. Rats were injected with insulin and killed, and then muscle and/or liver were used to prepare heatinactivated, deproteinized extracts. The extracts from insulin-stimulated rat tissues had one or more substances that inhibited protein kinase A (PKA) and activated GS phosphatase, compared with extracts from control rats. Insulin administration maintained PKA in muscle as an inactive holoenzyme, presumably desensitized to cAMP by the soluble second D 1 6 ( 1 1 -1 2 ) 5 4 3 -5 5 1 , N Classical actions of insulin involve increased glucose uptake from the bloodstream and its metabolism in peripheral tissues, the most important and relevant effects for human health. However, nonoxidative and oxidative glucose disposal by activation of glycogen synthase (GS) and mitochondrial pyruvate dehydrogenase (PDH) remain incompletely explained by current models for insulin action. Since the discovery of insulin receptor Tyr kinase activity about 25 years ago, the dominant paradigm for intracellular signaling by insulin invokes protein phosphorylation downstream of the receptor and its primar...

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Section: R E V I E W a R T I C L E M O L M Esupporting

confidence: 53%

D-Chiro-Inositol Glycans in Insulin Signaling and Insulin Resistance

Larner

Brautigan

Thorner

2010

Mol Med

158

156

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“…20) This inconsistency is probably due to the metabolic conversion of MI to other inositol derivatives in the body. [17][18][19] Under our experiment conditions, MI, at least in part, would be converted to D-chiro-inositol and lead to the stimulation of GLUT4 translocation in skeletal muscle and to a decrease in the plasma glucose level. Pak et al 17) have shown that the conversion of labeled […”

Section: Discussionmentioning

confidence: 98%

“…16) It has been reported that MI can be converted to chiro-inositol in such insulin-sensitive tissues as skeletal muscle, adipose tissue and liver. 13,[17][18][19] Our previous study demonstrated that inositol derivatives other than MI stimulated the glucose uptake in rat L6 myotubes. 20) The results from an immunoblot analysis revealed that at least D-chiro-, L-chiro-, epi-and muco-inositol, and PI stimulated GLUT4 translocation to the plasma membrane in L6 myotubes and also in the skeletal muscle of rats ex vivo.…”

mentioning

confidence: 99%

D-Pinitol andmyo-Inositol Stimulate Translocation of Glucose Transporter 4 in Skeletal Muscle of C57BL/6 Mice

Dang¹,

Mukai²,

Yoshida³

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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“…Moreover, as compared with healthy controls, urinary DCI excretion was found significantly reduced in impaired glucose tolerance, in first‐degree type 2 diabetes subjects' relatives, and in type 2 diabetes subjects, whereas the Myo‐inositol excretion was elevated . In addition, urinary excretion of the DCI progressively decreases from subjects with normal glucose tolerance to subjects with impaired glucose tolerance and subjects with diabetes . In contrast, Ostlund et al observed that DCI clearance was selectively elevated in both non–insulin‐dependent and insulin‐dependent diabetic subjects when compared with clearance of Myo.…”

Section: Inositol Molecular and Metabolic Aspectsmentioning

confidence: 95%

Inositol and antioxidant supplementation: Safety and efficacy in pregnancy

Formoso

Baldassarre

Ginestra

et al. 2019

Diabetes Metabolism Res

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Summary Pregnancies complicated by diabetes have largely increased in number over the last 50 years. Pregnancy is characterized by a physiologic increase in insulin resistance, which, associated with increased oxidative stress and inflammations, could induce alterations of glucose metabolism and diabetes. If not optimally controlled, these conditions have a negative impact on maternal and foetal outcomes. To date, one can resort only to diet and lifestyle to treat obesity and insulin resistance during pregnancy, and insulin remains the only therapeutic option to manage diabetes during pregnancy. However, in the last years, in a variety of experimental models, inositol and antioxidants supplementation have shown insulin‐sensitizing, anti‐inflammatory, and antioxidant properties, which could be mediated by some possible complementary mechanism of action. Different isomers and multiple combinations of these compounds are presently available: Aim of the present review article is to examine the existing evidence in order to clarify and/or define the effects of different inositol‐ and antioxidant‐based supplements during pregnancy complicated by insulin resistance and/or by diabetes. This could help the clinician's evaluation and choice of the appropriate supplementation regimen.

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Determination of UrinaryMyo-/Chiro-Inositol Ratios from Korean Diabetes Patients

Cited by 15 publications

References 21 publications

D-Chiro-Inositol Glycans in Insulin Signaling and Insulin Resistance

D-Chiro-Inositol Glycans in Insulin Signaling and Insulin Resistance

D-Pinitol andmyo-Inositol Stimulate Translocation of Glucose Transporter 4 in Skeletal Muscle of C57BL/6 Mice

Inositol and antioxidant supplementation: Safety and efficacy in pregnancy

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