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Acetyl carnitine AND angiotensin

Beatrice Bortolato, Kamilla W Miskowiak, Cristiano A Köhler, Michael Maes, Brisa S Fernandes, Michael Berk, André F Carvalho
BACKGROUND: Cognitive dysfunction in major depressive disorder (MDD) encompasses several domains, including but not limited to executive function, verbal memory, and attention. Furthermore, cognitive dysfunction is a frequent residual manifestation in depression and may persist during the remitted phase. Cognitive deficits may also impede functional recovery, including workforce performance, in patients with MDD. The overarching aims of this opinion article are to critically evaluate the effects of available antidepressants as well as novel therapeutic targets on neurocognitive dysfunction in MDD...
January 22, 2016: BMC Medicine
Daniela Macconi, Luca Perico, Lorena Longaretti, Marina Morigi, Paola Cassis, Simona Buelli, Norberto Perico, Giuseppe Remuzzi, Ariela Benigni
BACKGROUND: Angiotensin II promotes insulin resistance. The mechanism underlying this abnormality, however, is still poorly defined. In a different setting, skeletal muscle metabolism and insulin signaling are regulated by Sirtuin3. OBJECTIVE: Here, we investigate whether angiotensin II-induced insulin resistance in skeletal muscle is associated with Sirtuin3 dysregulation and whether pharmacological manipulation of Sirtuin3 confers protection. STUDY DESIGN: Parental and GLUT4-myc L6 rat skeletal muscle cells exposed to angiotensin II are used as in vitro models of insulin resistance...
2015: PloS One
Asieh Hosseini, Mohammad Abdollahi
Diabetic neuropathy (DN) is a widespread disabling disorder comprising peripheral nerves' damage. DN develops on a background of hyperglycemia and an entangled metabolic imbalance, mainly oxidative stress. The majority of related pathways like polyol, advanced glycation end products, poly-ADP-ribose polymerase, hexosamine, and protein kinase c all originated from initial oxidative stress. To date, no absolute cure for DN has been defined; although some drugs are conventionally used, much more can be found if all pathophysiological links with oxidative stress would be taken into account...
2013: Oxidative Medicine and Cellular Longevity
Carlos E Prada, John L Jefferies, Michelle A Grenier, Christina M Huth, Kimberley I Page, Robert L Spicer, Jeffrey A Towbin, Nancy D Leslie
Malonyl coenzyme A (CoA) decarboxylase (MCD) deficiency is a rare autosomal recessive organic acidemia characterized by varying degrees of organ involvement and severity. MCD regulates fatty acid biosynthesis and converts malonyl-CoA to acetyl-CoA. Cardiomyopathy is 1 of the leading causes of morbidity and mortality in this disorder. It is unknown if diet alone prevents cardiomyopathy development based in published literature. We report a 10-month-old infant girl identified by newborn screening and confirmed MCD deficiency with a novel homozygous MLYCD mutation...
August 2012: Pediatrics
Diana Revenco, James P Morgan
At present the prevalence of heart failure rises along with aging of the population. Current heart failure therapeutic options are directed towards disease prevention via neurohormonal antagonism (beta-blockers, angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers and aldosterone antagonists), symptomatic treatment with diuretics and digitalis and use of biventricular pacing and defibrillators in a special subset of patients. Despite these therapies and device interventions heart failure remains a progressive disease with high mortality and morbidity rates...
May 2009: Journal of Cellular and Molecular Medicine
Anura P Jayasooriya, Michael L Mathai, Lesley L Walker, Denovan P Begg, Derek A Denton, David Cameron-Smith, Gary F Egan, Michael J McKinley, Paula D Rodger, Andrew J Sinclair, John D Wark, Harrison S Weisinger, Mark Jois, Richard S Weisinger
In addition to its role in the storage of fat, adipose tissue acts as an endocrine organ, and it contains a functional renin-angiotensin system (RAS). Angiotensin-converting enzyme (ACE) plays a key role in the RAS by converting angiotensin I to the bioactive peptide angiotensin II (Ang II). In the present study, the effect of targeting the RAS in body energy homeostasis and glucose tolerance was determined in homozygous mice in which the gene for ACE had been deleted (ACE(-/-)) and compared with wild-type littermates...
May 6, 2008: Proceedings of the National Academy of Sciences of the United States of America
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