By Christos S. Mantzoros (auth.), Christos S. Mantzoros (eds.)
Nutrition and Metabolism: Underlying Mechanisms and scientific effects brings jointly the world over famous specialists to comprehensively evaluation our present knowing of the way foodstuff interacts with the genetic substrate in addition to environmental-exogenous components, together with actual job or the inability thereof, to lead to insulin resistance and the metabolic syndrome. After featuring the scope of the matter, the 1st significant a part of the booklet is dedicated to genetics and pathophysiology, the second one a part of the publication provides the general public wellbeing and fitness point of view of the main commonplace difficulties linked to meals and the metabolic syndrome, while the 3rd significant a part of the booklet makes a speciality of scientific overview and administration of the most sickness states linked to beside the point foodstuff and the metabolic syndrome. ultimately, basic info priceless for either clinicians and researchers alike is gifted within the Appendix. food and Metabolism: Underlying Mechanisms and scientific outcomes bargains the reader an up to date and authoritative evaluate of the key medical and scientific facets of the overlapping parts among food and metabolism.
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Additional resources for Nutrition and Metabolism: Underlying Mechanisms and Clinical Consequences
Org). Such programs comprising both academic and industrial partners, aim to study gene–environment interactions and thus identify genetic determinants susceptible to environmental stimuli that are capable of influencing obesity development. , genetics, transcriptomics, peptidomics, and metabolomics) coupled with clinical data will have a predominant role in elucidating the perturbed functions leading to obesity, and ultimately in developing better targeted therapies. In the context of the metabolic syndrome development, a study of 303 elderly twin pairs recently showed that glucose intolerance, obesity, and low HDL-cholesterol concentrations are significantly higher among monozygotic twins than among dizygotic twins, Fig.
In particular, the genetic characterization of naturally occurring obese animal models, such as ob/ob, db/db, fat and tubby mice, led to the discovery of recessive mutations in the genes encoding leptin (Lep or ob), leptin receptor (Lepr or db), carboxypeptidase E (Cpe, or fat), and tubby (Tub) (5,6). Furthermore, the latest murine obesity gene map identified 248 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes affecting body weight and adiposity (7). Transfer of this knowledge to clinical cases has confirmed the role of the above genes in human monogenic obesity and uncovered the critical role of the leptin/melanocortin pathway in the regulation of energy homeostasis (8).
22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 29 endocrine defects, decreased sympathetic tone, and immune system dysfunction indicate new targets for leptin action, greater central than peripheral resistance to the effects of leptin, and spontaneous correction of leptin-mediated defects. J. Clin. Endocrinol. Metab. 1999; 84:3686–3695. Clement K, Vaisse C, Lahlou N, et al. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature 1998; 392:398–401.
Nutrition and Metabolism: Underlying Mechanisms and Clinical Consequences by Christos S. Mantzoros (auth.), Christos S. Mantzoros (eds.)