Glucose Tolerance Factor – Insulin Mimetic and Potentiating Agent – A Source for a Novel Anti Diabetic Medication

Mirsky, Nitsa

doi:10.5772/54350

Cited by 2 publications

(9 citation statements)

References 71 publications

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“…Normally it is expressed in retinal astrocytes, but under pathologic conditions like hyperglycemia or ischemia, GFAP can be detected in other retina's areas like Muller cells layer. A remarkable reduction in GFAP expression was demonstrated in retinas derived from diabetic animals treated with GTF, where GFAP could be seen only in the glial astrocytes layer, very similar to what was found for healthy retinas [Mirsky, 2012], Additional studies from our laboratory detected the activity of sodium potassium ATPase, which is a marker forneuronal integrity, in retinas of healthy, diabetic, and diabetic rats treated with GTF, with a remarkably reduced activity in the diabetic retinas. This enzyme inactivation was prevented by GTF treatment: retinas removed from GTF treated rats showed restored sodium potassium ATPase activity [Mirsky, 2012].…”

Section: Introductionsupporting

confidence: 75%

“…In vitro studies with partially purified preparations of GTF showed stimulation of glucose metabolism in several tissues: GTF potentiated glucose oxidation to CO 2 in adipocytes [Anderson et al, 1978;Davies et al, 1985]and adipose tissue [Evans et al, 1973;Toepfer et al, 1977]. Several groups found an increased glucose transport to cardiomyocytes [Fischer et al, 1992], to yeast cells [Mirsky and Berdicevsky, 1994], and to adipocytes and myocytes [Weksler-Zangen et al, 2012], by the addition of GTF.Our group examined the oral administration of GTF in animal models for both types of diabetes, and found high and rapid anti-diabetic, hypolipidemic and antioxidant activity in diabetic untreated retinas [Mirsky, 2012],with a remarkable reduction in the complications of diabetes: nephropathy [Nakhoul et al, 2006],and retinopathy [Mirsky, 2012].In addition, in vitro studies showed insulin mimetic and insulin potentiating activity for GTF [Weksler-Zangen et al, 2012;Mirsky, 2012],…”

Section: Introductionmentioning

confidence: 84%

“…We have studied healthy, diabetic, and diabetic rats treated for two weeks with GTF, and demonstrated large amount of Glial Fibrillary Acidic Protein (GFAP) staining in Muller cell layer in diabetic untreated retinas [Mirsky, 2012].GFAP has been widely used as a cellular marker for retinal pathology. Normally it is expressed in retinal astrocytes, but under pathologic conditions like hyperglycemia or ischemia, GFAP can be detected in other retina's areas like Muller cells layer.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Glucose Tolerance Factor (GTF) on cerebral cells alterations in Diabetic rats

Shehadeh¹,

Sela²,

Palzur³

et al. 2015

AIJB

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Diabetes mellitus can lead to neuropathy and to cerebral cell death. Previously we showed that oral intake of Glucose Tolerance Factor (GTF) extracted from yeast reduced blood glucose and inhibited nephropathy and retinopathy in diabetic rats. The aim of our study wasto evaluates the effects of diabetes on neurodegenerative processes in rat's brain and to examine the influence of GTF treatment on these parameters. Diabetes was induced by streptozotocin (STZ). Diabetic rats were divided into 3 groups: Healthy, Diabetic untreated, and Diabetic treated with GTF. The hippocampus, known as the most sensitive area in the brain to the deleterious effects of diabetes, was studied. Cerebral apoptotic cell death was evaluated by immunohistochemistry using the TUNELassay, anti-glial fibrilary acidic protein (GFAP), and anti-neuron nucleus (NeuN) immunostaining. Blood glucose levels were remarkably increased in the STZ diabetic rats (healthy: 111.1+15.51, diabetic: 471.6+26.32 mg/dl),and significantly decreased to 352+20.49mg/dlin GTF treated group. The number of TUNEL stained apoptotic cells was significantly higher in diabetic rats compared to healthy and diabetic treated with GTF. Our data shows that programmed cell death is increased in the hippocampus of diabetic rats, but can be decreased by an oral treatment withGTF.

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Section: Introductionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

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Effect of Glucose Tolerance Factor (GTF) on cerebral cells alterations in Diabetic rats

Shehadeh¹,

Sela²,

Palzur³

et al. 2015

AIJB

Self Cite

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“…We showed in our previous studies 29,30 that GTF activated key proteins along insulin signaling pathway, exhibiting insulin mimetic potential. Based on these findings we anticipate an insulin-like activity of GTF also on Na/K ATPase pump.…”

Section: Discussionmentioning

confidence: 99%

“…29 Our review on GTF summarizes the research done on the subject. 30 Despite the high importance of GTF, its composition and molecular structure have not been revealed yet, mainly due to the lability of the purified fractions.…”

Section: Introductionmentioning

confidence: 99%

Featured Article: Inhibition of diabetic cataract by glucose tolerance factor extracted from yeast

Mirsky

Cohen

Eliaz

et al. 2016

Exp Biol Med (Maywood)

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Diabetes leads to many complications; among them is the development of cataract. Hyperglycemia brings to increased polyol concentration in the lens, to glycation of lens proteins, and to elevated level of ROS (Reactive Oxygen Species) causing oxidative stress. The glucose tolerance factor (GTF) was found by several groups to decrease hyperglycemia and oxidative stress both in diabetic animals and humans. The aim of our study was to explore the damages induced by high glucose to the eye lens and to assess the protective effects of GTF both in vivo and in vitro. The in vivo study included control healthy rats, streptozotocin (STZ) diabetic untreated rats, and STZ diabetic rats orally treated with 15 doses of GTF. The diabetic untreated rats developed cataracts, whereas the development of cataract was totally or partially prevented in GTF treated animals. In vitro studies were done on bovine lenses incubated for 14 days. Half of the lenses were incubated in normal glucose conditions, and half in high glucose conditions (450 mg%). To one group of the normal or high glucose condition GTF was added. The optical quality of all the lenses was measured daily by an automated scanning laser system. The control lenses, whether with or without GTF addition, did not show any reduction in their quality. High glucose conditions induced optical damage to the lenses. Addition of GTF to high glucose conditions prevented this damage. High glucose conditions affected the activity of aldose reductase and sodium potassium ATPase in lens epithelial cell. Addition of GTF decreased the destructive changes induced by high glucose conditions. The amount of soluble cortical lens proteins was decreased and structural changes were detected in lenses incubated in high glucose medium. These changes could be prevented when GTF was added to high glucose medium. Our findings demonstrate the anticataractogenic potential of GTF.

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Glucose Tolerance Factor – Insulin Mimetic and Potentiating Agent – A Source for a Novel Anti Diabetic Medication

Cited by 2 publications

References 71 publications

Effect of Glucose Tolerance Factor (GTF) on cerebral cells alterations in Diabetic rats

Effect of Glucose Tolerance Factor (GTF) on cerebral cells alterations in Diabetic rats

Featured Article: Inhibition of diabetic cataract by glucose tolerance factor extracted from yeast

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