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There is an increase in the incidence and prevalence of type-2 diabetes and obesity which leads to the structural and functional changes in myocardium leading to a lethal complication called diabetic cardiomyopathy (DCM). In the present study, we investigated the preventive effect of cinnamon (3% of Cinnamomum zeylanicum bark powder in AIN-93 diet for 3 months) feeding on DCM and the concerned mechanisms in a rodent model. Experimental diabetes was induced by a single intraperitoneal injection of 40 mg/kg b.w streptozotocin (STZ), 15 min after the ip administration of 60 mg/kg b.w of nicotinamide (NA) in Wistar-NIN (WNIN) male rats. The oxidative stress parameters were investigated by assessing superoxide dismutase (SOD), glutathione-s-transferase (GST) enzyme activity, protein carbonyls and malondialdehyde (MDA) levels. The histopathology of myocardium was analyzed by H&E and Masson’s trichrome staining, and scanning electron microscopy. The changes in diabetic rat heart involved the altered left ventricular parietal pericardium, structural changes in myocardial cells, enhanced oxidative stress. Masson’s trichrome and H&E staining have shown increased fibrosis, and perinuclear vacuolization in NA-STZ induced diabetic rat myocardium. Cinnamon feeding prevented the oxidative stress and myocardial alterations in the heart of diabetic rats. Taken together, these results suggest that cinnamon can effectively prevent the metabolic and structural changes in NA-STZ induced diabetic cardiomyopathy.

The rapid increase in global diabetes burden with its associated morbidity and mortality is a major health concern for humans. Prediabetes is a condition which predispose a person not only to diabetes but also to the associated complications including morbidity even in the absence of an apparant hyperglycemia. However, appropriate dietary intervention may not only prevent but also improve one’s condition as diet is the major contributor to such metabolic disorders. Here, we investigated the effect of dietary ginger (Zingiber officinale Roscoe) on the markers of insulin resistance and pathophysiology in a diet-induced prediabetic rat model. Male Sprague-Dawley (SD) rats were fed the following diets: control (5% groundnut oil + 65 % corn starch), high fat high fructose (HFHF; 25% beef tallow + 35 % fructose) and HFHF with 3 % ginger (HFHFG) for eight months. Plasma markers of insulin resistance, lipid profile, oral glucose tolerance (OGTT; 2nd and 5th month), intraperitoneal insulin tolerance (ITT), plasma total antioxidant capacity (TAC), liver histology and pancreatic immunohistochemistry (IHC) were examined. The impaired OGTT, ITT and insulin sensitivity indices with observed hyperinsulinemia and hypertriglyceridemia suggest that HFHF feeding resulted in prediabetes in rats. HFHF feeding also decreased insulin secretion in the pancreas, increased lipid accumulation in liver and total oxidants in plasma. The effects of HFHF feeding on glucose regulation, pathophysiology of pancreas and liver; total oxidative stress were improved by ginger feeding. The present study demonstrated thatlong-term HFHF feeding induces prediabetes in experimental rats while dietary ginger neutralizes the HFHF induced impairment in glucose regulation, dyslipidemia, and oxidative stress.

Objective We assessed the effect of a daily intake of a micronutrient-fortified beverage for 14 mo on indicators of biochemical status of important micronutrients in schoolchildren. Methods A double-blind, placebo-controlled, matched-pair, cluster, randomization study design was used. Biochemical indicators of micronutrient status were evaluated at baseline and at the end of 14 mo on a subsample in nine matched pairs. Prevalence (percentage) of subclinical deficiency, mean, and mean increments of each indicator were compared between supplemented and placebo groups. Results Extent of inadequacy at baseline was more or less 100% for folic acid, 65% for vitamins B2 and B6, and 55% for vitamins C and A. Prevalence of anemia among subjects was 55%, with inadequacy of vitamin B12 being 40% and that of vitamin D being 30%. No subject had inadequacy of iodine based on urinary iodine. Supplementation of a micronutrient-enriched beverage for 14 mo significantly improved the status of many of the nutrients. The effect was significant with respect to vitamins A, B2, and B12, folic acid, vitamin D, parathyroid hormone, and thyroid-stimulating hormone in children who received the supplement compared with those who received only placebo. Hemoglobin status improved only in children who had anemia in the supplemented group. Conclusions Prevalence of multiple subclinical micronutrient deficiencies are high in middle-income Indian school children. Daily consumption of a micronutrient-enriched beverage had positive effects that were confined to those nutrients that were inadequate at baseline.

Accumulation of advanced glycation endproducts (AGE) from nonenzymatic glycation of proteins has been implicated in several diabetic complications including diabetic cataract. Previously, we have reported that extracts of dietary agents such as cinnamon have the potential to inhibit AGE formation. In this study, we have shown procyanidin-B2 as the active component of cinnamon that is involved in AGE inhibition using bioassay-guided fractionation of eye lens proteins under in vitro conditions. The data indicate that procyanidin-B2 enriched fraction scavenges dicarbonyls. Further, procyanidin-B2 fraction of cinnamon inhibited the formation of glycosylated hemoglobin in human blood under ex vivo conditions. We have also demonstrated the physiological significance of procyanidin-B2 fraction in terms of delay of diabetic cataract through inhibition of AGE in diabetic rats. These findings establish the antiglycating potential of procyanidin-B2 fraction of cinnamon which suggests a scope for controlling AGE-mediated diabetic complications by food sources that are rich in proanthocyanidins like procyanidin-B2.

There is increasing evidence that complications related to diabetes are associated with increased oxidative stress. Curcumin, an active principle of turmeric, has several biological properties, including antioxidant activity. The protective effect of curcumin and turmeric on streptozotocin (STZ)-induced oxidative stress in various tissues of rats was studied.Three-month-old Wistar-NIN rats were made diabetic by injecting STZ (35 mg/kg body weight) intraperitoneally and fed either only the AIN-93 diet or the AIN-93 diet containing 0.002% or 0.01% curcumin or 0.5% turmeric for a period of eight weeks. After eight weeks the levels of oxidative stress parameters and activity of antioxidant enzymes were determined in various tissues.STZ-induced hyperglycemia resulted in increased lipid peroxidation and protein carbonyls in red blood cells and other tissues and altered antioxidant enzyme activities. Interestingly, feeding curcumin and turmeric to the diabetic rats controlled oxidative stress by inhibiting the increase in TBARS and protein carbonyls and reversing altered antioxidant enzyme activities without altering the hyperglycemic state in most of the tissues.Turmeric and curcumin appear to be beneficial in preventing diabetes-induced oxidative stress in rats despite unaltered hyperglycemic status.

Curcumin, the active principle of turmeric, has been shown to have both antioxidant and hypoglycemic activity in vitro and in vivo. The purpose of this study was to investigate the effect of curcumin on the onset and maturation of galactose induced cataract.Sprague-Dawley rats (21 days old) were divided into 5 groups. The control group (A) received an AIN-93 diet, the galactose group (B) received 30% galactose in the diet, the test groups (C and D) received the B group diet plus 0.002% and 0.01% curcumin respectively, and group (E) received the control diet plus 0.01% curcumin, all for a period of 4 weeks. Cataract progression due to galactose feeding was monitored by slit lamp microscope and classified into 4 stages. At the end of the experiment biochemical parameters such as lipid peroxidation, aldose reductase (AR), sorbitol dehydrogenase (SDH), reduced glutathione, protein content, and protein carbonyls were measured in the lens. Advanced glycated end products (AGE) and protein oxidation were measured by AGE and tryptophon fluorescence respectively. Crystallin profile was analyzed by size exclusion chromatography (HPLC).Slit lamp microscope observations indicated that curcumin at 0.002% (group C) delayed the onset and maturation of cataract. In contrast even though there was a slight delay in the onset of cataract at the 0.01% level (group D), maturation of cataract was faster when compared to group B. Biochemical analysis showed that curcumin at the 0.002% level appeared to exert antioxidant and antiglycating effects, as it inhibited lipid peroxidation, AGE-fluorescence, and protein aggregation. Though the reasons for faster onset and maturation of cataract in group D rats was not clear, the data suggested that under hyperglycemic conditions higher levels of curcumin (0.01%) in the diet may increase oxidative stress, AGE formation, and protein aggregation. However, feeding of curcumin to normal rats up to a 0.01% level did not result in any changes in lens morphology or biochemical parameters.These results suggest that curcumin is effective against galactose-induced cataract only at very low amounts (0.002%) in the diet. On the other hand at and above a 0.01% level curcumin seems to not be beneficial under hyperglycemic conditions, at least with the model of galactose-cataract.