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      Role of carnitine in disease

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          Abstract

          Carnitine is a conditionally essential nutrient that plays a vital role in energy production and fatty acid metabolism. Vegetarians possess a greater bioavailability than meat eaters. Distinct deficiencies arise either from genetic mutation of carnitine transporters or in association with other disorders such as liver or kidney disease. Carnitine deficiency occurs in aberrations of carnitine regulation in disorders such as diabetes, sepsis, cardiomyopathy, malnutrition, cirrhosis, endocrine disorders and with aging. Nutritional supplementation of L-carnitine, the biologically active form of carnitine, is ameliorative for uremic patients, and can improve nerve conduction, neuropathic pain and immune function in diabetes patients while it is life-saving for patients suffering primary carnitine deficiency. Clinical application of carnitine holds much promise in a range of neural disorders such as Alzheimer's disease, hepatic encephalopathy and other painful neuropathies. Topical application in dry eye offers osmoprotection and modulates immune and inflammatory responses. Carnitine has been recognized as a nutritional supplement in cardiovascular disease and there is increasing evidence that carnitine supplementation may be beneficial in treating obesity, improving glucose intolerance and total energy expenditure.

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          Emerging role of polyphenolic compounds in the treatment of neurodegenerative diseases: a review of their intracellular targets.

          Aging is the major risk factor for neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. A large body of evidence indicates that oxidative stress is involved in the pathophysiology of these diseases. Oxidative stress can induce neuronal damages, modulate intracellular signaling, ultimately leading to neuronal death by apoptosis or necrosis. Thus antioxidants have been studied for their effectiveness in reducing these deleterious effects and neuronal death in many in vitro and in vivo studies. Increasing number of studies demonstrated the efficacy of polyphenolic antioxidants from fruits and vegetables to reduce or to block neuronal death occurring in the pathophysiology of these disorders. These studies revealed that other mechanisms than the antioxidant activities could be involved in the neuroprotective effect of these phenolic compounds. We will review some of these mechanisms and particular emphasis will be given to polyphenolic compounds from green tea, the Ginkgo biloba extract EGb 761, blueberries extracts, wine components and curcumin.
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            Impaired functional visual acuity of dry eye patients.

            To report dry eye patients' functional visual acuity, which was measured after sustained eye opening for 10-20 seconds, as a simulation of visual function of daily acts of gazing, which is defined as looking at an object with involuntary blink suppression. Interventional clinical nonrandomized comparative trial. We measured ordinary best-corrected visual acuity and functional visual acuity in non-Sjögren's syndrome (non-SS, N = 10) and Sjögren's syndrome (SS, N = 12) patients and in normal controls (N = 8), prospectively. Surface regularity index (SRI) of corneal topography was also measured under routine circumstances and after sustained eye opening. Blink rates while gazing were measured during reading in another 28 dry eye patients and during driving in another 8 normal controls. Functional visual acuity did not change (1.27-1.16) in normal controls, but decreased significantly from 1.18-0.336 in non-SS patients (P = .0007) and from 1.15-0.228 (P < .00001) in SS patients. SRI after sustained eye opening increased in non-SS (P = .032) and SS patients (P = .0007), but not in the normal controls. Blink rates during reading (P < .001) and driving (P = .012) were significantly decreased from baseline blink rates. This study shows that the visual function of dry eye patients becomes abnormal with ocular surface irregularity when the eye is kept open for 10-20 seconds. Our data indicate impaired visual function in dry eye patients while gazing. Functional visual acuity may be important in daily activities.
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              Central administration of oleic acid inhibits glucose production and food intake.

              The hypothalamus and other regions within the central nervous system (CNS) link the sensing of nutrients to the control of metabolism and feeding behavior. Here, we report that intracerebroventricular (ICV) administration of the long-chain fatty acid oleic acid markedly inhibits glucose production and food intake. The anorectic effect of oleic acid was independent of leptin and was accompanied by a decrease in the hypothalamic expression of neuropeptide Y. The short-chain fatty acid octanoic acid failed to reproduce the metabolic effects of oleic acid, and ICV coadministration of inhibitors of ATP-sensitive K(+) channels blunted the effect of oleic acid on glucose production. This is the first demonstration that fatty acids can signal nutrient availability to the CNS, which in turn limits further delivery of nutrients to the circulation.
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                Author and article information

                Journal
                Nutr Metab (Lond)
                Nutrition & Metabolism
                BioMed Central
                1743-7075
                2010
                16 April 2010
                : 7
                : 30
                Affiliations
                [1 ]Institute for Eye Research, Sydney, New South Wales, Australia
                [2 ]Allergan Inc, Irvine, CA, USA
                [3 ]School of Optometry and Vision Science, University of New South Wales, Sydney, Australia
                Article
                1743-7075-7-30
                10.1186/1743-7075-7-30
                2861661
                20398344
                535ce7f5-2c95-4c77-8e74-62916942cb92
                Copyright ©2010 Flanagan et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 17 December 2009
                : 16 April 2010
                Categories
                Review

                Nutrition & Dietetics
                Nutrition & Dietetics

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