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Undurti N Das

Publications and source records attributed to Undurti N Das.

61 records · Page 4Linked to original sources
PubMed2002

Effect of anti-oxidants, free radical quenchers and cyclo-oxygenase inhibitor on benzo(a)pyrene-induced suppression of human lymphocyte mitogenesis in vitro.

BACKGROUND: Benzo(a)pyrene (BP) is a known carcinogen and immunosuppressor. Activation of BP to its reactive intermediates is cyclo-oxygenase (COX) dependent and occurs via a free radical dependent mechanism. The aim of this study was to know whether anti-oxidants, free radical quenchers and (COX) inhibitor, indomethacin, influence the suppression of human T cells induced by BP in vitro. MATERIAL/METHODS: Human lymphocytes, obtained from healthy human volunteers, were stimulated to proliferate using phytohaemagglutinin (PHA). The effect of vitamin E, SOD, catalase, mannitol, and COX-inhibitor, indomethacin, on BP-induced suppression of human T cell proliferation was evaluated. RESULTS: Except for catalase, a hydrogen peroxide (H2O2) radical quencher, none of the agents tested could inhibit BP-induced suppression of human T cell proliferation in vitro. CONCLUSIONS: BP-induced suppression of human T cell proliferation is probably, induced by increased production of H2O2. Prostaglandins and superoxide anion and hydroxyl radical do not seem to participate in BP-induced human T cell growth suppression.

Antioxidants↗
PubMedDate not supplied

A surgical rat model of human Roux-en-Y gastric bypass.

Obesity affects 30% of the United States population and its detrimental effects are obesity-related metabolic diseases. For patients refractory to conventional weight loss therapy, gastric bypass surgery is one of the proven methods for inducing a sustained weight loss and reversing the metabolic sequelae of obesity. To understand the mechanisms of weight loss and the amelioration of related metabolic comorbid conditions, a reproducible animal model is needed. We report our developmental experience with rat models of sequential Roux-en-Y gastric bypass after reproducing the diet-induced obesity that characterizes the hallmarks of human obesity. Four experiments were performed to induce weight reduction through successive modifications: In Experiment 1 a 20% stapled gastric pouch with a 16 cm biliary-pancreatic limb and a 10 cm alimentary limb accomplished sufficient weight loss within 10 days to ameliorate metabolic changes associated with obesity, but the occurrence of gastrogastric fistulas prevented sustained weight loss; in Experiment 2 the model was improved by dividing the stomach to avoid gastrogastric fistula, but again sustained weight loss was not achieved; in Experiment 3 the biliary-pancreatic limb was lengthened from 16 to 30 cm, reducing the common channel to approximately 18 cm. Sustained weight loss was achieved for 28 days. In Experiment 4 the model in Experiment 3 was modified by dividing the stomach between two rows of staples. Sustained weight loss was observed for 67 days. We developed a reproducible rat model of Roux-en-Y gastric bypass. The existence of this model opens a new field of research in which to study the metabolic sequelae of obesity and the mechanisms of weight loss.

Anastomosis, Roux-en-Y↗
PubMedDate not supplied

A perinatal strategy to prevent coronary heart disease.

I investigated whether metabolism of essential fatty acids and the concentrations of their long-chain metabolites (long-chain polyunsaturated fatty acids [LCPUFAs]) are altered in fetal or perinatal growth retardation, maternal hypercholesterolemia, low-grade systemic inflammation, insulin resistance, and atherosclerosis, conditions that predispose to the development of coronary heart disease (CHD).I critically reviewed the literature pertaining to the metabolism of essential fatty acids in CHD and conditions that predispose to it.LCPUFAs enhance endothelial nitric oxide synthesis, suppress the production of the proinflammatory cytokines tumor necrosis factor and interleukin-6, attenuate insulin resistance, and have antiatherosclerotic properties. Low-birthweight infants have decreased concentrations of LCPUFAs, especially arachidonic acid. Neonatal arachidonic acid status is related to intrauterine growth, and LCPUFAs improve fetal and postnatal growth. LCPUFAs are useful in the management of hyperlipidemia, inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, and may mediate the beneficial actions of statins. Plasma concentrations of various LCPUFAs are low in diabetes mellitus, hypertension, and CHD and in populations at high risk of CHD. Breast milk is rich in LCPUFAs, and this may explain why and how adequate (6 mo to 1 y) breast feeding protects against the development of obesity, hypertension, insulin resistance, and CHD.LCPUFAs are essential for the growth and development of the fetus and infant. LCPUFAs can prevent various conditions that predispose to the development of CHD. The low incidence of CHD seen in adequately breast-fed infants can be linked to the LCPUFA content of breast milk. Based on this evidence, I suggest that provision of LCPUFAs during critical periods of growth, especially from the second trimester of pregnancy to age 5 y, prevents CHD in adult life.

Arteriosclerosis↗
PubMedDate not supplied

Is type 2 diabetes mellitus a disorder of the brain?

I propose that type 2 diabetes mellitus is due to damage to neurons in the ventromedial hypothalamus or to a defect in the action or properties of insulin or insulin receptors in the brain. These neuronal abnormalities are probably secondary to a marginal deficiency of long-chain polyunsaturated fatty acids during the critical periods of brain growth and development. Hence, supplementation of adequate amounts of long-chain polyunsaturated fatty acids during the third trimester of pregnancy to 2 y postterm can prevent or postpone the development of diabetes mellitus.

Acetylcholine↗
PubMedDate not supplied

Folic acid says NO to vascular diseases.

OBJECTIVES: The possible link between folic acid or folate and tetrahydrobiopterin (H(4)B), vitamin C, polyunsaturated fatty acids (PUFAs), and nitric oxide (NO), which may explain the beneficial actions of these nutrients in various vascular conditions, was investigated. METHODS: The literature pertaining to the actions of folic acid/folate, H(4)B, vitamin C, PUFAs, and NO was reviewed. RESULTS: Impaired endothelial NO (eNO) activity is an early marker for cardiovascular disease. Most risk factors for atherosclerosis are associated with impaired endothelium-dependent vasodilatation due to reduced NO production. Folate not only reduces plasma homocysteine levels but also enhances eNO synthesis and shows anti-inflammatory actions. It stimulates endogenous H(4)B regeneration, a cofactor necessary for eNO synthesis, inhibits intracellular superoxide generation, and thus enhances the half-life of NO. H(4)B in turn enhances NO generation and augments arginine transport into the cells. Folic acid increases the concentration of omega-3 PUFAs, which also enhance eNO synthesis. Vitamin C augments eNO synthesis by increasing intracellular H(4)B and stabilization of H(4)B. Insulin stimulates H(4)B synthesis and PUFA metabolism, suppresses the production of proinflammatory cytokine tumor necrosis factor-alpha and superoxide anion, and enhances NO generation. The ability of folate to augment eNO generation is independent of its capacity to lower plasma homocysteine levels. CONCLUSIONS: The common mechanism by which folic acid, H(4)B, vitamin C, omega-3 fatty acids, and L-arginine bring about their beneficial actions in various vascular diseases is by enhancing eNO production. Hence, it remains to be determined whether a judicious combination of folic acid, vitamins B12, B6, and C, H(4)B, L-arginine, and omega-3 fatty acids in appropriate amounts may form a novel approach in the prevention and management of various conditions such as hyperlipidemias, coronary heart disease, atherosclerosis, peripheral vascular disease, and some neurodegenerative conditions.

Antioxidants↗