Decreased Insulin-Mediated but Not Non-Insulin-Dependent Glucose Disposal Rates in Glucose Intolerance and Type II Diabetes in African (Ghanaian) Immigrants

A novel black tea decoction containing vanadate has successfully replaced insulin in a rat model of insulin-dependent diabetes but is untested in non-insulin-dependent diabetic animals. A tea-vanadate decoction (TV) containing 30 or 40 mg sodium orthovanadate was administered by oral gavage to two groups of Zucker diabetic fatty rats and a conventional water vehicle containing 30 or 40 mg of sodium orthovanadate to two others. In the latter group receiving the 30-mg dose, vanadate induced diarrhea in 50% of the rats and death in 10%. In contrast, TV-treated rats had no incidence of diarrhea and no deaths. Symptoms were more severe in both groups with higher vanadate doses, so these were discontinued. After ~16 weeks, the level of vanadium in plasma and tissue extracts was negligible in a further group of untreated rats but highly elevated after vanadate treatment. Vanadium levels were not significantly different between the TV-treated diabetic rats and the diabetic rats given vanadate in a water vehicle. Over the 115 days of the study, blood glucose levels increased from ~17 to 25 mmol/L in untreated diabetic rats. This was effectively lowered (to <10 mmol/L) by TV treatment. Fasting blood glucose levels were 5, 7, and 20 mmol/L in control (nondiabetic, untreated), TV-treated and untreated diabetic rats, respectively. Rats required treatment with TV for only ~50% of the days in the study. Increase in body mass during the study was significantly lower in untreated diabetic rats (despite higher food intake) than the other groups. Body mass gain and food intake were normal in TV-treated rats. Water intake was 28 mL/rat daily in control rats, 130 mL/rat daily in untreated diabetic rats, and 52 mL/rat daily in TV-treated diabetic rats. Plasma creatinine and aspartate aminotransferase levels were significantly depressed in untreated diabetic rats, and TV treatment normalized this. Our results demonstrate that a novel oral therapy containing black tea and vanadate possesses a striking capacity to regulate glucose and attenuates complications in a rat model of type II diabetes. Key words: diabetes mellitus, tea, glycemia, type II diabetes.

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The Nutritional Therapy of Non-Insulin Dependent (Type II) Diabetes

The Diabetes Educator ◽

10.1177/014572178300900317 ◽

1983 ◽

Vol 9 (3) ◽

pp. 59-59

Keyword(s):

Type Ii Diabetes ◽

Nutritional Therapy ◽

Type Ii ◽

Insulin Dependent ◽

Dependent Type

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Enhanced external counterpulsation (EECP) decreases advanced glycation end products and proinflammatory cytokines in patients with non-insulin-dependent type II diabetes mellitus for up to 6 months following treatment

Acta Diabetologica ◽

10.1007/s00592-016-0869-6 ◽

2016 ◽

Vol 53 (5) ◽

pp. 753-760 ◽

Cited By ~ 2

Author(s):

Paloma D. Sardina ◽

Jeffrey S. Martin ◽

Wojciech K. Dzieza ◽

Randy W. Braith

Keyword(s):

Diabetes Mellitus ◽

Type Ii Diabetes ◽

Type Ii Diabetes Mellitus ◽

Type Ii ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products ◽

Insulin Dependent ◽

Enhanced External Counterpulsation ◽

Dependent Type

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PHYLOGENESIS, ETIOLOGY AND PATHOGENESIS OF INSULIN RESISTANCE. DIFFERENCES FROM TYPE II DIABETES MELLITUS

Annals of the Russian academy of medical sciences ◽

10.15690/vramn.v67i4.202 ◽

2012 ◽

Vol 67 (4) ◽

pp. 65-73

Author(s):

V. N. Titov

Keyword(s):

Diabetes Mellitus ◽

Insulin Resistance ◽

Fatty Acids ◽

Hormonal Regulation ◽

Type Ii Diabetes ◽

Type Ii Diabetes Mellitus ◽

Type Ii ◽

Insulin Dependent ◽

The One

We believe that etiological factor of insulin resistance is phylogenetically late formation of insulin and its specific functionality, i.e., providing energy substrates for the biological function of locomotion. According to biological subordination, insulin cannot change regulation formed at the early stages of phylogenesis in all cells, including those that become insulin-dependent at the late stages of phylogenesis. This involves a) β-oxidation of fatty acids in the mitochondria, b) synthesis of С 16:0 palmitic saturated fatty acid, c) glucose metabolism in pro- and eukaryotes, d) regulation of biochemical reactions in insulin-independent cells, e) humoral effects of mediators at the level of paracrine cell communities which are structural and functional units of all internal organs, and f) hormonal regulation at the entire organism level. Pathogenetic factors of insulin resistance are biochemical and functional disorders occurring in vivo upon activation of biological functions and reactions that formed phylogenetically earlier than insulin. During phylogenesis the insulin system has intrinsically built up over the regulatory mechanisms of mitochondria, early unicellular organisms and paracrine cell communities. Insulin functionally interacts with them all, but it cannot abolish the effects of any phylogenetically earlier humoral mediator. Insulin resistance is a pathophysiological disparity between humoral regulation of metabolism at the level of phylogenetically earlier paracrine cell communities and at the level of phylogenetically late total organism, on the one hand, and successive phylogenetic formation of passive cellular uptake of fatty acids as unesterified fatty acids and later triglycerides, on the other. If insulin resistance results from changes in the primary structure of transport proteins, in glucose storage and cellular insulin reception, it can be referred to as type II diabetes mellitus.

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