Genetic and molecular understanding for the development of methionine-rich maize: a holistic approach.

Maize (Zea mays) is the most important coarse cereal utilized as a major energy source for animal feed and humans. However, maize grains are deficient in methionine, an essential amino acid required for proper growth and development. Synthetic methionine has been used in animal feed, which is costlier and leads to adverse health effects on end-users. Bio-fortification of maize for methionine is, therefore, the most sustainable and environmental friendly approach. The zein proteins are responsible for methionine deposition in the form of δ-zein, which are major seed storage proteins of maize kernel. The present review summarizes various aspects of methionine including its importance and requirement for different subjects, its role in animal growth and performance, regulation of methionine content in maize and its utilization in human food. This review gives insight into improvement strategies including the selection of natural high-methionine mutants, molecular modulation of maize seed storage proteins and target key enzymes for sulphur metabolism and its flux towards the methionine synthesis, expression of synthetic genes, modifying gene codon and promoters employing genetic engineering approaches to enhance its expression. The compiled information on methionine and essential amino acids linked Quantitative Trait Loci in maize and orthologs cereals will give insight into the hotspot-linked genomic regions across the diverse range of maize germplasm through meta-QTL studies. The detailed information about candidate genes will provide the opportunity to target specific regions for gene editing to enhance methionine content in maize. Overall, this review will be helpful for researchers to design appropriate strategies to develop high-methionine maize.

Implications of magnesium deficiency in type 2 diabetes: a review.

Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. It plays a fundamental role as a cofactor in various enzymatic reactions involving energy metabolism. Magnesium is a cofactor of various enzymes in carbohydrate oxidation and plays an important role in glucose transporting mechanism of the cell membrane. It is also involved in insulin secretion, binding, and activity. Magnesium deficiency and hypomagnesemia can result from a wide variety of causes, including deficient magnesium intake, gastrointestinal, and renal losses. Chronic magnesium deficiency has been associated with the development of insulin resistance. The present review discusses the implications of magnesium deficiency in type 2 diabetes.

Effect of a low magnesium diet on in vitro glucose uptake in sucrose fed rats.

Dietary magnesium deficiency and excess sucrose in the diet have been shown to play an important role in the development of insulin resistance. This study is an extension of a previously published experiment (Magnes Res 2004; 17: 293-300) and is focused on the effect of a low magnesium diet on in vitro glucose uptake in sucrose fed rats. For this purpose male Wistar rats were divided into four groups and fed control, high sucrose, low magnesium and high sucrose low magnesium diets for a period of three months. Serum and erythrocyte magnesium values demonstrated a significant drop in the low magnesium and high sucrose low magnesium groups. A significant increase was observed in the body weight of the high sucrose group, whereas the weights of animals in the high sucrose low magnesium group remained unchanged from controls. The biochemical analysis showed a significant decrease in in vitro glucose uptake in liver, muscle and diaphragm of rats consuming high sucrose, low magnesium and high sucrose low magnesium diets. The maximum reduction, however, was observed in the combined high sucrose low magnesium group. These findings seem to suggest the potential of a high sucrose low magnesium diet to cause insulin resistance by reducing glucose uptake in target tissues of rats.

Implications of oxidative stress in high sucrose low magnesium diet fed rats.

BACKGROUND: Magnesium deficiency as well as excess sucrose in the diet have been shown to be associated with the generation of reactive oxygen species (ROS). AIM OF THE STUDY: In the present study we have investigated the combined effect of low magnesium high sucrose diet on the development of oxidative stress in rats. METHODS: Male Wistar rats were divided into four groups and fed control (C), low magnesium (LM), high sucrose (HS) and low magnesium high sucrose (HSLM) diet for a period of 3 months. Levels of various antioxidants, viz. ascorbic acid, vitamin E, uric acid, glutathione and non-protein thiols were determined along with malondialdehyde levels (lipid peroxidation marker). Anti-oxidant enzyme activities were determined in livers of experimental diet fed animals. RESULTS: Compared to controls, significantly increased lipid peroxidation was observed in plasma and liver tissue of animals in the three experimental groups, however, the combined HSLM group showed greater lipid peroxidation. Levels of various antioxidants fell significantly in plasma and tissue of LM, HS and HSLM rats. Total thiols as well as liver non-protein thiols followed a similar trend with the greatest drop in anti-oxidant potential seen in the HSLM rats. The activities of the anti-oxidant enzymes viz. SOD, GST and catalase also declined considerably in test animals w.r.t controls, with the HSLM group showing the lowest activities. CONCLUSION: These findings suggest that a diet low in magnesium and high in sucrose causes oxidative stress in rats, as reflected by increased lipid peroxidation and reduced anti-oxidant potential.

Effect of vitamin E supplementation on diabetes induced oxidative stress in experimental diabetes in rats.

Diabetes induced by streptozotocin (50 mg/kg body wt, i.p.) in the rats substantially increased the plasma glucose and malondialdehyde levels along with corresponding decrease in the antioxidants levels. Supplementation of vitamin E (200 mg/kg body wt., ip) for 5 weeks resulted in non-significant decrease in the blood glucose levels but plasma malondialdehyde levels were reduced to below normal levels. Plasma vitamin E, vitamin C, uric acid and red blood cell glutathione levels were also restored to near normal levels on vitamin E supplementation to diabetic rats as compared to control (diabetic) rats. The activities of antioxidant enzymes, catalase (EC 1.11.1.6), glutathione peroxidase (GSHPx EC 1.11.1.9), and glutathione reductase (GR EC 1.6.4.2) were also concomitantly restored to near normal levels by vitamin E supplementation to diabetic rats. The results clearly demonstrated that vitamin E supplementation augments the antioxidant defense mechanism in diabetes and provides evidence that vitamin E may have a therapeutic role in free radical mediated diseases.

Effect of magnesium supplementation on oxidative stress in alloxanic diabetic rats.

Magnesium deficit and oxidative stress are common features of the diabetic state. This concept supported by another observation that magnesium deficiency is also a state of increased oxidative stress prompted us to study the effect of magnesium supplementation on magnesium status and oxidative stress in diabetic rats. For this purpose, male Wistar rats were made diabetic with a single intraperitoneal injection of Alloxan. Experimental diabetes caused a significant decrease in serum and red blood cell magnesium levels and increased urinary excretion of magnesium. Marked increase in plasma malondialdehyde and corresponding decrease in vitamins C & E, uric acid and total thiols was observed in the diabetic rats as compared to control group. In liver, MDA levels were increased significantly with concomitant decrease in vitamin C, non-protein thiols and antioxidant enzymes (SOD & GST). Magnesium supplementation for four weeks restored serum and RBC magnesium levels to near normal levels with marginal but significant decrease in blood glucose levels. Plasma and liver MDA levels were reduced significantly and vitamin C and total thiols were increased significantly with magnesium supplementation. Antioxidant enzyme activity was also increased significantly with magnesium supplementation in diabetic rats. Our data clearly demonstrates that alloxanic diabetes is associated with decreased magnesium status and increased oxidative stress and that magnesium supplementation can in part restore the antioxidant parameters and decrease the oxidative stress in experimental diabetic rats.