Current Nutrition & Food Science - Volume 4, Issue 2, 2008

Abdominal obesity, atheroslcerosis, insulin resistance, hyperlipidemias, hypertension, and type 2 diabetes mellitus are important components of metabolic syndrome X. An increase in pro-inflammatory cytokines, decrease in the concentrations of endothelial nitric oxide (eNO) and adiponectin, and an alteration in hypothalamic peptides that control satiety, hunger, and food intake have been reported in metabolic syndrome X. Although when and how metabolic syndrome X is initiated is not clear, there is evidence to suggest that increased consumption of high-energy diet, saturated and trans-fats by pregnant women and lactating mothers could trigger changes in the concentrations of long-chain polyunsaturated fatty acids (LCPUFAs) in maternal and fetal plasma and tissues. LCPUFAs have a modulatory influence on neuronal growth, maturation and synapse formation; influence the actions of hypothalamic peptides, neuropeptides, leptin, adiponectin, and various cytokines, especially during the perinatal period. In addition, LCPUFAs function as endogenous inhibitors of HMG-CoA reductase and ACE (angiotensin converting enzyme), augment eNO synthesis, modulate vascular tone, and potentiate insulin action both in the peripheral tissues and brain. Hence, sub-optimal maternal and fetal plasma and tissue concentrations of LCPUFAs increase pro-inflammatory cytokine levels that could trigger the development of metabolic syndrome X in those children who have a genetic predisposition, and continue to take highenergy diet, and saturated and trans-fats. This implies that perinatal interventions in the form of adequate supplementation of LCPUFAs could be of significant benefit in the prevention of metabolic syndrome X. Preliminary evidence suggests that supplementation of LCPUFAs can restore the levels of hypothalamic peptides to normal. In addition, weight loss due to Roux-en-gastric bypass procedure done in diet-induced obese animals decreased inflammation, restored hypothalamic “body weight/ appetite/ satiety set point” by restoring hypothalamic neuropeptides to normal, suggesting a cross talk between gastrointestinal hormones and hypothalamus. These evidences suggest that metabolic syndrome X occurs in a genetically predisposed subject as a result of interaction(s) between hypothalamic peptides, gastrointestinal tract, cytokines, nutrition, and life style factors.

Microbial metabolism in the human colon impacts on health and disease. Production of intermediate metabolites and end-products depends largely on the supply of dietary carbohydrates, including prebiotics (fructooligosaccharides) and functional foods (resistant starch), that resist small intestinal digestion. Colonic bacteria ferment these substrates to a wide range of products, predominantly short-chain fatty acids, including metabolites that can be either deleterious (e.g. D-lactate, sulphides) or beneficial (e.g. butyrate) to gut health. Lactate accumulation in the colon has been associated with gastrointestinal disturbance, for example in severe ulcerative colitis, whereas in the healthy state lactate is efficiently utilised by gut bacteria. Understanding the interaction between microbial metabolism and dietderived nutrient supply is crucial for maintaining a healthy metabolic balance in the colon. Prediction of such nutritional responses can be achieved by integrating in mathematical models information from stable isotope studies, that quantify metabolite flows, and molecular techniques, that accurately determine changes in microbial composition diversity. From such approaches, better nutritional advice can be provided in order to improve gut health. Furthermore, such understanding can be used to manipulate and improve the action of prebiotics and probiotics.

Carotenoids are commonly present exclusively in flora and microbes where they perform critical functions in photosynthesis and photoprotection. These lipophilic molecules are not synthesized by vertebrates and invertebrates. Carotenoids are recognized as high-value antioxidant food supplements and their antioxidant activity may be higher than β-carotene and ??-tocopherol leading to a prevention of lipid peroxidation. In addition, other beneficial effects of carotenoids are well established. These include reduction in gastric inflammation, bacterial load reduction in H-pylori infected humans and mice, age related macular degeneration, prevention of carcinogenesis, atherosclerosis, cardiovascular ailments etc. Epidemiology and clinical studies have shown that each carotenoid has its own individual characteristics. For example β-cryptoxanthin has been shown to be potent in lung cancer and lycopene is inversely associated with prostate cancer and astaxanthin inhibits LDL oxidation. Over 700 natural carotenoids with diverse molecular structures have been identified with potential medical benefits. However, only a handful of carotenoids, such as α-carotene, β- carotene, astaxanthin, β-cryptoxanthin, lycopene, canthaxanthin, lutein and zeaxanthin have been explored for their health benefits. Leutin and zeaxanthin are commonly found in human fluids including macula. This review summarizes role of these two carotenoids in age related macular degeneration.

Taurine (2-Amino ethane sulfonic acid) is a naturally occurring sulphur amino acid, found in several mammalian and non mammalian tissues. Taurine is believed to be involved in several life processes. Its deficiency is a cause of concern in developing abnormalities in many organs like eye, heart, kidney, brain etc during developmental stages and even later on. Taurine contents are believed to be high in bone tissue mostly due to accumulation by transport, as taurine synthesis in bone is yet to be recorded. A strong stimulating role of taurine in bone matrix formation and collagen synthesis has been observed in osteoblast like UMR-106 cells; together with this, inhibition of bone resorption and osteoclast formation by taurine has also been identified, making taurine an agent for preventing inflammatory bone resorption in periodontal diseases. Thus, taurine acts as a double beneficial agent; stimulating bone formation and inhibiting bone loss. Along with these actions in bone, it also has beneficial action in radio protection, wound healing, bone gain through exercise and many others. Taurine has the potential to replace bisphosphonates; suitable taurine analogues may further accelerate this. An extensive analytical study of taurine contents in both the stages of bone formation and bone loss may make taurine as a single marker of bone metabolism. However taurine-bone interaction needs more deep study towards regulation of taurine, interaction with ions, and many other pharmacological and physiological actions. An in depth clinical study of its actions in bone may make taurine an ideal agent for desired effect; yet, all these recorded taurine - bone interactions, are milestones for future research.

This review of current medical knowledge about the etiology, evaluation, medical, and pharmacologic treatment of obesity suggests patient care strategies emphasizing office evaluation and treatment. Office assessment of obesity, which is the consequence of multiple genetic, neurohormonal, environmental, and behavioral factors, should include a careful chronological history with calculation of body mass index and a focused examination. Treatment consideration should be given to recommendations about calorie intake, but debate continues over the ideal macronutrient composition. Other treatment recommendations for successful weight loss and maintenance include a high level of physical activity, behavior modification programs that improve adherence to diet and exercise, and pharmacologic therapy. Obesity is an increasingly prevalent medical problem in the United States that is best treated using a multidisciplinary approach. Medical providers require the most up-to-date information in order to provide their patients with a multifaceted approach to successful weight loss and lifelong weight maintenance.