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Anti-Aging Gene linked to Appetite Regulation Determines Longevity in Humans and Animals



The process of aging is determined by various genetic and environmental factors. Aging is associated with increased oxidative stress that alters cellular chromatin structure, DNA methylation with histone modifications. These epigenetic alterations lead to nuclear changes associated with mitochondrial apoptosis that is a major defect in the global chronic disease epidemic (1). The variability in longevity between individuals in different communities implicate various nutritional and environmental factors involved in transcriptional dysregulation that lead to cell damage that accumulates with age and contributes to mitophagy, insulin resistance and programmed cell death. The absence or malfunction of a gene (2) necessary for transcriptional regulation of gene expression, DNA repair and telomere maintenance in neurons has become essential with relevance to neurodegeneration that determines aging and lifespan in man and animals.
*Correspondence to Author:
Dr Ian Martins, School of Medical
Sciences, Edith Cowan University,
Western Australia 6009, Australia,
Ph: +61863042574,
How to cite this article:
Ian James Martins. Anti-Aging
Gene linked to Appetite Regulation
Determines Longevity in Humans
and AnimalsInternational Journal of
Aging Research, 2018, 1:6.
eSciPub LLC, Houston, TX USA.
Ian James Martins, IJOAR, 2018 1:6
International Journal of Aging Research
Editorial Article IJOAR (2018) 1:6
Anti-Aging Gene linked to Appetite Regulation Determines
Longevity in Humans and Animals
The process of aging is determined by various genetic and envi-
ronmental factors. Aging is associated with increased oxidative
stress that alters cellular chromatin structure, DNA methylation
with histone modications. These epigenetic alterations lead to
nuclear changes associated with mitochondrial apoptosis that
is a major defect in the global chronic disease epidemic (1). The
variability in longevity between individuals in different commu-
nities implicate various nutritional and environmental factors in-
volved in transcriptional dysregulation that lead to cell damage
that accumulates with age and contributes to mitophagy, insulin
resistance and programmed cell death. The absence or malfunc-
tion of a gene (2) necessary for transcriptional regulation of gene
expression, DNA repair and telomere maintenance in neurons
has become essential with relevance to neurodegeneration that
determines aging and lifespan.
Key words: longevity; species; appetite; immune system; hu-
man; mitophagy; animals; neurodegneration; Sirtuin 1; nutritional
Ian James Martins
aCentre of Excellence in Alzheimer’s Disease Research and Care, Sarich Neuroscience Research
Institute, Edith Cowan University, Verdun Street, Nedlands, 6009, Western Australia, Australia;
bSchool of Psychiatry and Clinical Neurosciences, The University of Western Australia, Nedlands,
6009; cMcCusker Alzheimer’s Research Foundation, Hollywood Medical Centre, 85 Monash Ave-
nue, Suite 22, Nedlands, 6009, Australia
Ian James Martins, IJOAR, 2018 1:6
Major implementations in lifestylestyle changes
have been conducted and to introduce calorie
restriction that alters cell metabolism by the use
of specific nutrients to improve immunity
connected to longevity (3). Genes that
determine premature lifespan in humans have
been identified and include genes (3,4) such as
breast cancer genes BRCA1 and BRCA2 and
hyperlipidemia genes (the low-density
lipoprotein receptor, apolipoprotein B). Four
candidate genes (3) have been implicated in
longevity such as apolipoprotein E, angiotensin-
converting enzyme, histocompatibility locus
antigen and plasminogen activator inhibitor 1.
These genes have effects on longevity in
animals and humans by effects of calorie
restriction (5) that determine the function of
homeostatic proteins with effects on nutrient
metabolism and immunity. A genome-wide scan
has identified new loci for exceptional longevity
and reveal a genetic overlap between longevity
and age-related diseases and traits that include
coronary artery disease and Alzheimer's disease
(6). In humans and animals (dogs, cats, bears,
horses, elephants, livestock/cattle) lifespan can
vary between 29-86 years and in man depending
on the community human lifespan can reach a
maximum of 104 years with average age (70-80
years). Centenarians have very low levels of
chromosome abnormalities (7) and indicate the
absence of the malfunction in genes associated
with DNA repair and DNA methylation that
prevent mitochondrial apoptosis linked to
various chronic diseases such as diabetes and
neurodegenerative diseases. An anti-aging
gene (8) that determines longevity and lifespan
in various species
(Figure 1) has been identified as Sirtuin 1 (Sirt
1). Sirt 1 is a nicotinamide adenine dinucleotide
(NAD +) dependent class III histone deacetylase
(HDAC) that targets transcription factors
(peroxisome proliferator-activated receptor-
gamma coactivator, p53, pregnane x receptor)
to adapt gene expression to metabolic activity
and as a deacetylase is involved in the
deacetylation of the nuclear receptors critical to
neuron proliferation, insulin resistance and non
alcoholic fatty liver disease (1). Sirt 1 is involved
in telomere maintenance and DNA repair with its
critical involvement chromosome stability and
cell proliferation. Sirt 1 is important to the
regulation of other anti-aging genes such as
klotho, p66shc and Forkhead box protein O1
with relevance to age related diseases (8).
Figure 1. In humans and animals Sirt 1 is the
anti-aging/heat shock gene that is sensitive to
heat/cold stress with relevance to the induction
of mitochondrial apoptosis and autoimmune
disease. Sirt 1 regulates food intake and is the
calorie sensitive gene that determines species
survival linked to diabetes and
neurodegenerative diseases.
Major interests in appetite regulation has
indicated that appetite control is critical to
longevity and lifespan and connected to various
chronic diseases (9). Sirt 1 as a heat shock gene
is important to the immune system in various
species (10) with its repression linked to
autoimmune disease (11). Core body
temperature dysregulation will inactivate Sirt 1
and induce mitochondrial apoptosis with
relevance to autoimmune disease and species
longevity (12). Diet, environment and lifestyle
(stress) changes incriminate Sirt 1 as the
defective gene (Figure 1) involved in aging and
lifespan and associated with neurodegeneration
and chronic disease. In animals food quality (13)
is essential to maintain Sirt 1 expression and
activity with relevance to regulation of core body
temperature and autoimmune disease. The
longevity of lifespan in cattle and livestock will be
determined by the xenobiotic content (10) and
Ian James Martins, IJOAR, 2018 1:6
food end products from bacteria/fungus such as
bacterial lipopolysaccharides and mycotoxins
(14). Animals may be more sensitive to
neurodegeneration and synaptic plasticity with
dietary interventions essential to maintain
neuron and synapse interactions (14). The role
of caffeine and Indian Spices (15,16) in food
products has become of interest and may
determine longevity in man. Furthermore
inactivation of Sirt 1 is associated with
senescence and its role in antimicrobial activity
and mitophagy (17) may be critical for the
survival of animal
In humans the function of the anti-aging gene
Sirt 1 is critical to the maintenance of other
longevity and anti-aging genes involved with
aging and lifespan. Appetite regulation is
connected to Sirt 1 function with mitochondrial
apoptosis and neurodegeneration linked to
various chronic diseases. Food consumption in
the cattle and livestock industry should be
carefully controlled since Sirt 1 and its
dysregulation may be more sensitive to
mitochondrial apoptosis in animals with effects
on neurodegeneration and synaptic plasticity
that determines species longevity.
This work was supported by grants from Edith
Cowan University, the McCusker Alzheimer's
Research Foundation and the National Health
and Medical Research Council.
1. Ian James Martins. Genomic Medicine and Acute
Cardiovascular Disease Progression in Diabetes.
International Journal of Medical Studies.
2. Sandra Rodríguez-Rodero, Juan Luis Fernández-
Morera, Edelmiro Menéndez-Torre, Vincenzo
Calvanese, Agustín F. Fernández, Mario F. Fraga.
Aging Genetics and Aging. Aging and Disease.
3. Giuseppe Passarino, Francesco De Rango,
Alberto Montesanto. Human longevity: Genetics or
Lifestyle? It takes two to tango. Immunity and
Ageing. 2016;13:(12):1-6.
4. Nir Barzilai, Alan R. Shuldiner. Searching for
Human Longevity Genes: The Future History of
Gerontology in the Post-genomic Era. Journal of
Gerontology, 2001;56A(2):M83M87.
5. Michal Jazwinski. Longevity, Genes, and Aging.
Science. 1996;27(5271):54-59.
6. Kristen Fortney, Edgar Dobriban, Paolo
Garagnani, Chiara Pirazzini, Daniela Monti,
Daniela Mari, Gil Atzmon, Nir Barzilai, Claudio
Franceschi, Art B. Owen, Stuart K. Kim. Genome-
Wide Scan Informed by Age-Related Disease
Identifies Loci for Exceptional Human Longevity.
PLOS Genetics, 2015; 11(12): e1005728
7. Diddahally Govindaraju, Gil Atzmonb, Nir Barzilai.
Genetics, lifestyle and longevity: Lessons from
centenarians. Applied and Translational
Genomics. 2015;4:23-32.
8. Ian James Martins. Anti-Aging Genes Improve
Appetite Regulation and Reverse Cell Senescence
and Apoptosis in Global Populations. Advances in
Aging Research, 2016; 5:9-26.
9. Ian James Martins. Appetite dysregulation and
obesity in Western Countries Ian J Martins · Edited
by Emma Jones,; LAP LAMBERT Academic
Publishing. 2013;1-80.
10. Ian James Martins. Single Gene Inactivation with
Implications to Diabetes and Multiple Organ
Dysfunction Syndrome. Journal of Clinical
Epigenetics. 2017;3(24): 1-8.
11. Ian James Martins. Appetite Control and
Biotherapy in the Management of Autoimmune
Induced Global Chronic Diseases. Journal of
Clinical Immunology and Research. 2018; 2(1): 1-
12. Ian James Martins. Regulation of Core Body
Temperature and the Immune System Determines
Species Longevity. Current Updates in
Gerontology. 2017; 1: (6.1):1-6.
13. Ian James Martins. Food quality induces a miscible
disease with relevance to Alzheimer’s disease and
Neurological diseases. Journal of Food
Research.2016; 5(6): 45-52.
14. Ian James Martins. Dietary Interventions Reverse
Insulin and Synaptic Plasticity Defects Linking to
Diabetes and Neurodegenerative Diseases. SL
Nutrition and Metabolism. 2017; 1(111)1-5.
15. Ian James Martins. Caffeine with Links to NAFLD
and Accelerated Brain Aging. Chapter: Non-
Alcoholic Fatty Liver Disease - Molecular Bases,
Prevention and Treatment. InTech - Open Science
Open Minds | InTechOpen. 2017.
Ian James Martins, IJOAR, 2018 1:6
16. Ian James Martins. Indian Spices and
Biotherapeutics in Health and Chronic Disease.
Health. 2018;10:374-380.
17. Ian James Martins. Antimicrobial activity
inactivation and toxic immune reactions induce
Epilepsy in human. Journal of Medical Discovery.
... Novel genes [36] have been identified that are involved with autoimmune disease [18,19,36, 37] and glucolipotoxicity with irreversible immune complications relevant to NAFLD, diabetes [3] and the pathogenetic loop. The discovery of the anti-aging gene Sirt 1 now has become important to the treatment of diabetes with insulin therapy in Type 1 and Type 2 diabetes connected to Sirt 1 activation in the pancreas with relevance to insulin release [38] with Sirt 1 associated with mitochondrial biogenesis (Figure 1) and cell survival in various tissues [38,39]. The inactivation of Sirt 1 [39] in humans leads to the pathogenetic loop in diabetes and implicates nutritional and environmental factors in the induction of programmed cell death. ...
... The discovery of the anti-aging gene Sirt 1 now has become important to the treatment of diabetes with insulin therapy in Type 1 and Type 2 diabetes connected to Sirt 1 activation in the pancreas with relevance to insulin release [38] with Sirt 1 associated with mitochondrial biogenesis (Figure 1) and cell survival in various tissues [38,39]. The inactivation of Sirt 1 [39] in humans leads to the pathogenetic loop in diabetes and implicates nutritional and environmental factors in the induction of programmed cell death. ...
... Insulin therapy has been used to improve liver function but with NAFLD, high dose insulin therapy may be unsuccessful with liver inflammation [40][41][42] associated with uncontrolled hyperglycemia and mitochondrial apoptosis (Figure 2). Insulin therapy with insulin dose and oral anti-diabetic medications should be re-evaluated to improve hepatocyte mitochondrial biogenesis with relevance to reversal of liver disease connected to hyperglycemia and NAFLD in various Type 1, Type 2 and Type 3 [35,39] diabetics. ...
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Non-alcoholic fatty liver disease (NAFLD) is a major medical challenge because of its increasing prevalence, difficulties in diagnosis, complex pathogenesis, and lack of approved therapies. In the near future, it will become the major form of chronic liver disease in adults and children and the leading indication for liver transplantation. It can be detected by noninvasive and invasive tools, and its treatment depends mainly on lifestyle modification to prevent disease progression and its related sequelae. This book provides information on NAFLD prevalence, etiology, pathogenesis, pathology, diagnosis, and treatment. Chapters cover such topics as experimental work related to the disease, other diseases related to NAFLD, and noninvasive tools for diagnosis
... For example, the role of the anti-aging gene Sirtuin 1 [2] may be critical to the survival of dairy cows, cattle and dairy buffalo. Sirtuin 1 [3] levels may need to be assessed with relevance key regulatory mechanisms and key gene functions that determine the molecular switch involved in the aging process [4,5] that may affect milk production and breeding programs. Heat and cold stress [6] affects Sirtuin 1 with core body temperature effects that may determine milk production and breeding of dairy cattle and buffalo. ...
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Animal growth is a coordinated developmental process that requires altering the expression of hundreds to thousands of genes to modify many biochemical and biological signaling cascades. The genetic analysis of economic traits and molecular breeding research are hotspots for animal husbandry and, in the case of Chinese dairy cattle, much progress has been made in recent years. Actually, the level of information of molecular events at the transcriptional, biochemical, hormonal, and metabolite levels underlying animal development process has increased considerably. The current review summarizes progress in research into the genetic basis of economic traits and molecular breeding of dairy cows, dual-purpose cattle and dairy buffalo, to better understand the molecular switch involved in development process with important consequences from a breeding point of view.
... Extracts from microalgae have various bioactive substances which accelerate the healing process and maintain skin moisture. In particular, the moisturizing effect and skin regeneration effect of microalgae fatty acid have been proven, making it a popular ingredient for cosmetics [18]. Studies were conducted at the gene level to determine the cause of anti-aging and skin regeneration. ...
... In most countries, ignorance of these diseases exposes older people to discrimination and exclusion. As various studies show, the ageing process and the increase in the number of elderly people in African countries may be also linked to the inactivation of anti-aging genes that are critical for cell survival in many tissues [24]. The global chronic disease epidemic [25][26][27] indicate that the inactivation of the anti-aging gene is linked to NAFLD (non-alcoholic fatty liver disease), diabetes and neurodegenerative diseases such as Alzheimer's disease. ...
... Diets that reverse NAFLD [11] are particularly important to maintain liver function and an intact immune system [12]. ...
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The World Health Organization on December 31, 2020 was informed by Chinese authorities of an outbreak of a novel strain of coronavirus called SARS-CoV-2. In February 20, 2020, nearly 167,500 COVID-19 cases have been documented and the virus has killed over 6,600 people. The role of anti-aging genes may be critical to prevent COVID-19 infection. In elderly people and individuals from the global chronic disease the anti-aging gene may be repressed with COVID-19 infection linked to accelerated programmed cell death and multiple organ disease syndrome.
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International Scientist Lifetime Achievement Award 2022 On Engineering, Science and Medicine. This Lifetime Achievement Awards recognizes contributions over the whole of a career of Ian James Martins. Dr Ian James Martins is also the Outstanding Scientist Award 2022, International Scientist Awards 2022 (INSO AWARDS) on Engineering, Science and Medicine. ABCD Wall provide a live platform of the Life Journey and career: Video Program: Live platform YouTube:
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The COVID-19 epidemic and global chronic disease epidemic is expected to cost Biomarker Research billion of dollars in the next 20 years. Biomarkers such as Sirtuin 1 are now relevant to the COVID-19 epidemic and chronic diseases such as diabetes, Alzheimer’s disease and neurodegenerative disease research. Sirtuin 1 may now be relevant to the COVID-19 pandemic with the Sirtuin 1 repression connected to severity of the COVID-19 disease with programmed cell death. The role of the anti-aging gene Sirtuin 1 is now critical to the success of therapy in COVID-19 ill individuals with relevance to myocardial infarction, lung disease and neurodegeneration and the improved survival in COVID-19 individuals. The role of diets, drugs and lifestyles may be critical in the reduction of the severity of the COVID-19 illness in the developing and developed world. The success of genomic medicine will be important to COVID-19 patients and Vaccine technologies. Strategies and therapy that target the immune system and Sirtuin 1 will reduce the severity of the COVID-19 epidemic and the risk of multiple organ disease syndrome in these infected individuals. Indian spices and relevance to the immune system as a booster may need to be reassessed with relevance to Sirtuin 1 repression versus activation.
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World's Famous Scientist Dr. Ian James Martins from Australia conferred with Honorary Degree of Doctor of Science for Outstanding Scientific Contribution in Nutrition. Dr. Ian Martins from Australia conferred with Honorary Degree of Doctor of Medicine for Outstanding Scientific Contribution in Diabetes. {Honoris Causa} International Press Release July 2020, Dr. Ian James Martins DSc (Honoris Causa) Doctrin De Science Award Honoris Causa. Top Peer Reveiwer 2019, Global Peer Reveiw Awards, PUBLONS, Editor/Reveiwer for Open Acess Pub/MDPI journals/other international journals. Advisory Board Member for Photon Journal. Fellow of International Agency for Standards and Ratings (IASR). Chief Editor for International Journal of Diabetes Research (2014-2020), Research and Reviews: Neuroscience (2016-2020) and Journal of Diabetes and Clinical Studies (2017-2020),Advancement in Case Studies (2020-2023), Novel Techniques in Nutrition and Food Sciences (2020-2023), Global Journal of Endocrinology and Metabolism (2020-2023), Interventions in Obesity and Diabetes (2020-2023), and Journal of Diabetes, Obesity and Metabolism. BIT Member (BIT Congress. Inc) with an H-index of 130, Google Scholar Citations (32),ResearchGate STATs (32), Scopus Mendeley (22), UWA Research Repository (18), Semantic Scholar (25), Publon (1). Scientist for The Science Advisory Board (USA) and an Academic with (4276 veiws, 497 public mentions). Postdoctoral Researcher Frontiers in Genetics (5251 veiws, 1359 downloads, 1373 citations), Dimensions (1547 citations). Editorial Board Member for 150 journals. The citations past 25 years have accumulated to >14874. Semantic Scholar Semantic Scholar profile with 133 highly influential citations RESEARCHGATE ANALYSIS: RG score (> 96%) of SCIENTISTS. ECU RESEARCH ONLINE (3164 downloads across 43 papers). Lifetime Membership by International Agency for Standards and Ratings as Fellow for Diabetes, Medical Science (Nutrition). Winner (World Academic Championship -2017) in Diabetes and Medical Science (Nutrition). 117 INTERNATIONAL Certificates from international conferences, congresses, summits and journals have been received in relation to anti-aging, health and disease. Keynote addresses at International Conference on Biomedicine and Pharmacotherapy 2018, Global Experts Meeting on Diabetes, Hypertension and Metabolic Syndrome 2018, Immunology World 2018, Laboratory Medicine 2018, Innovate Pharma 2017, Innovate Neurology 2017, World Diabetes and Endocrinology Summit-2017 and Pharmacology and Ethnopharmacology 2016. Chair Sessions on International Conference on Biomedicine and Pharmacotherapy 2018, Global Experts Meeting on Diabetes, Hypertension and Metabolic Syndrome 2018, Laboratory management, Cytogenetics, Clinical Microbiology, Diagnostic Laboratory Medicine etc, 13th Interantional Conference on Laboratory Medicine and Pathology, Berlin, Germany, June 25-26, 2018, Chairing Sessions on Vaccinology, Immunopathology, Immunotherapy, Immune Proteomics, Cancer and Tumour Oncology, 7th World Congress on Immunology, Amsterdam, Netherlands, April 19-20, 2018, Chair, Biotherapeutics for Diseases, Bit's 2nd International Congress of Biotherapy-2018 (Committee Member), Chair, Innovate Conferences 2017, Chair/Co-Chair at congress World Gene Convention-2016 (Shanghai, China, Pharmacology and Ethanopharmacology 2016 (Chicago, USA), Annual World Congress of Diabetes-2014 (Haikou, China), World Gene Convention-2014 (Haikou, China). Reveiwer/Editor for approx. 150 journals. Organizing Committee and Advisory Board Member for 170 International Conferences (2018-2020). APPROX. 400 IMPORTANT PUBLICATION ACHIEVEMENTS TRANSMITTED AND COLLECTED BY TWEET: Ian James Martins (@IanJamesMartin2) | Twitter BLOOD TEST for mitochondrial survival critical to metabolic disease in diabetes and neurodegenerative diseases. 1. Sirtuin 1, a Diagnostic Protein Marker and its Relevance to Chronic Disease and Therapeutic Drug Interventions. EC Pharmacology and Toxicology 6.4 (2018): 209-215. 2. Evaluation of diagnostic tests in human health and disease. J Clin Path Lab Med. 2018;2(1):13-15. SPECIAL FOCUS ON ADVANCES IN TREATING DISEASES Simplicity in complexity: Ian James Martins’ research on insulin therapy and autoimmune disease with a special focus on NAFLD. The Scientific News, Advances in Treating Diseases. November Edition, 2018. REPORTED BY Annie B. Coulter, RECEIVED BY WORLDWIDE AUDIENCE: 84,287,977, 2019. RELEVANT REFERENCE: Insulin Therapy and Autoimmune Disease with Relevance to Nonalcoholic Fatty Liver Disease. Non Alcoholic Fatty Liver Disease. An Update. IntechOpen. October, 2018.
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According to the endosymbiotic theory, mitochondria is an organelle derived from an ancient alpha-proteobacteria that developed a symbiosis with a eukaryotic ancestor. Mitochondrial DNA (mtDNA) exists in hundreds to thousands of copies in each cell and encodes for 13 structural proteins which are subunits of respiratory chain. Mitochondria generate energy for cellular processes by producing ATP through oxidative phosphorylation. Also, they control other processes as nucleotide and heme syntheses, redox balance, calcium metabolism, waste management (urea and ROS) and apoptosis. mtDNA deletions, point mutations, thymine dimers and mtDNA depletions are strongly related with disease in humans and other mammals. Some mtDNA alterations can arise spontaneously during life spam, other can be inherited by maternal lineage as specific mutations. So, nuclear DNA mutations can produce mitochondrial disorders because while mtDNA encodes 13 proteins, mitochondria need almost 2000 proteins with structural and functional roles. In these cases, a mendelian inheritance pattern can be observed. mtDNA alterations can be produced by exposure to toxic substances or UV and high-energy radiations. mtDNA mutations are cumulative because mitochondria lack reparative mechanisms. Normal and mutant mtDNA can coexist in the same cell, a condition known as heteroplasmy. Heteroplasmy allows the persistence of an otherwise lethal mutation through generations. Mitochondrial disorders can appear as myopathies, cardiomyopathies, lactic acidosis diabetes mellitus, female’s subfertility, lipodystrophy, neuropathies as autism or Alzheimer’s diseases or haematological and renal disorders. Due to heteroplasmy, these disorders can appear with a wide range of intensities, because the mutant mtDNA needed to cause a disorder varies among organisms, among organ systems and within a given tissue, and depends on a delicate balance between ATP supply and demand. Another kind of problem surges at tissues under hypoxemic-related damage, where mitochondria play an important role in cell survival and recovery. Finally, the role played by mitochondria in cancer survival and treatment is focused in many researches.Mitochondrial disorders have not a single treatment. In the most serious cases of inherited mitochondrial diseases, the supportive treatment only improves the life quality slightly. Nowadays, the most of experimental approaches search prevents the clinical manifestations of these diseases by reducing the mutant mtDNA percentage into the oocyte or the early embryo via nuclear transfer. Artificial Mitochondrial Transfer/Transplant (AMT/T) rises as an alternative to many acquired or inherited mitochondrial disorders, both ex vivo, in vitro and in vivo conditions. The present work shows the variation of an AMT/T method -MitoCeption- in a cellular model for in vitro treatment of acquired mtDNA disorder caused by UV Radiation by using Peripheral Blood Mononuclear Cells (PBMCs) and the feasibility of the same method for ex vivo AMT/T to murine oocytes and early embryos. In the in vitro model of cell damage by UV radiation, the main results represent an upgrading in the applications of AMT/T. We showed that PBMCs could be used as a primary allogeneic mixed source of mitochondria. We also showed that these mitochondria can be transferred in a mix from different donors (PAMM) to UVR-damaged, non-adherent primary cells. Additionally, the duration of the MitoCeption protocol was reduced. On the other hand, Mitoception used on murine oocytes and early embryos probed to be a safe method for AMT/T by using human mitochondrial mix (PAMM). Murine 0ocytes’ and embryos’ exogenous mitochondrial content was observed by fluorescence microscopy and exogenous mtDNA was quantified by qPCR and 2ΔCT method. Finally, healthy murine new-borns were obtained by embryo transfer, probing that human mitochondria were removed from murine cells during embryo’s development after implantation.
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Human survival and the immune system are now relevant to the global chronic disease epidemic that involves NAFLD, cardiovascular disease and diabetes. Chronic disease assessment require measurement of plasma Sirt 1 levels with relevance to autoimmune disease and mitophagy. Biotherapy that involves immunotherapy may stabilize mitophagy that is connected to autoimmune disease and the early induction of global chronic diseases. Appetite control is essential to maintain Sirt 1 levels and to prevent the generation of immunogenic lipids and proteins that induce programmed cell death. Autoimmune disease and immunometabolism defects are now connected to the primary induction of mitophagy with the acceleration of chronic diseases in the developed and developing world.
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The acceleration in the rate of chronic disease that involves insulin resistance has become of concern in various countries. The rate of the most prevalent chronic diseases involves the metabolic syndrome and non alcoholic fatty liver disease (NAFLD) that is closely associated to diabetes and neurodegenerative diseases. Biotherapeutics and nutritional biotherapy have become important to reverse these global diseases. Biotherapeutics that involves Indian spice therapy requires assessment with relevance to insulin therapy, immunotherapy, antimicrobial therapy and drug therapeutics. Combined insulin therapy and Indian spice therapy regulates human insulin biological activity with relevance to the prevention of uncontrolled intracellular glucose levels and mitochondrial apoptosis. Biotherapeutics with nutritional biotherapy that involves the use of various nutrients such as magnesium and phosphatidylinositol (gm/day) is essential to insulin therapy. Factors such as stress, core body temperature and food quality influence biotherapeutics and Indian spice therapy with delayed spice clearance associated with mitochondrial dysfunction (cell apoptosis) and altered drug/caffeine therapy with relevance to the global diabetes pandemic.
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Nutritional diets are essential to prevent nonalcoholic fatty liver disease (NAFLD) in the global obesity and diabetes epidemic. The ingestion of palmitic acid-rich diets induces NAFLD in animal and human studies. The beneficial properties of olive oil (oleic acid) may be superseded by ingestion of palmitic acid-rich diets. Hepatic caffeine metabolism is regulated by palmitic and oleic acid with effects of these fats on amyloid beta metabolism. Healthy fats such as olive oil may facilitate rapid amyloid beta clearance in the periphery to maintain drug therapy in diabetes and various neurological diseases. Repression of the anti-aging gene sirtuin 1 (Sirt 1) prevents the beneficial properties of olive oil. Brain disorders induce NAFLD and supersede caffeine’s therapeutic effects in the prevention of NAFLD. Delayed hepatic caffeine metabolism in NAFLD and increased caffeine transport to the brain with aging-induced mitophagy in neurons with induction of type 3 diabetes and neurodegenerative disease.
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Nutritional genomics and regulation of Sirt 1 has become important to the treatment of diabetes and the progression of various organ diseases. Sirt 1 inactivation by heat/cold stress interrupts HSPs metabolism connected to defective immunometabolism and mitophagy. Science and medicine and its relevance to genomic medicine needs to consider Sirt 1 gene expression with its relevance to diabetes and accelerated immune reactions that cause acute cardiovascular disease. Factors such as caffeine, body temperature and pollution need to be considered as the trigger for acute cardiovascular disease associated with the progression of NAFLD and diabetes.
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The calorie sensitive gene Sirtuin 1 (Sirt 1) determines nitric oxide (NO) homeostasis and immunosenescence relevant to the induction of various chronic diseases in human and other species. Appetite control is essential to Sirt 1 function for preventing adipose tissue transformation (adipocytokine release), non alcoholic fatty liver disease (NAFLD) and the development of epilepsy. Sirt 1 repression by bacterial lipopolysaccharides (LPS) leads to delayed hepatic clearance of anti-microbial drugs with relevance to mitophagy, neuron apoptosis and interference with antimicrobial/antiepileptic drug therapy. Increased absorption of LPS from food/water induces magnesium deficiency with inactivation of antimicrobial/antiepileptic drug therapy. Heat and cold stress alters Sirt 1’s role in cell cholesterol dyshomeostasis associated with increased heat shock proteins (HSP) involved with inactivation of antimicrobial proteins and promotion of the cytotoxic immune response. The genetics of immunity that determines immune competence changes over a human’s life span and involves the gene Sirt 1 that has antimicrobial properties by its regulation of NO metabolism connected to the immune system, mitophagy and epilepsy.
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Nutritional and environmental epigenetics are involved with the repression of anti-aging genes that are linked to the chronic disease epidemic. Unhealthy diets inactivate the calorie sensitive gene Sirtuin 1 (Sirt 1) involved in epigenetic processes that promote immune system alterations, mitochondrial apoptosis, Non-alcoholic Fatty Liver Disease (NAFLD), diabetes and Nitric Oxide (NO) modification with relevance to core body temperature involved with appetite regulation, glucose homeostasis and hepatic xenobiotic metabolism. The interplay between NO and epigenetics has attracted interest with relevance to autoimmune disease and mitophagy that has become of critical concern to diabetes and the development of MODS. Future research involved with nutritional research and the maintenance of Sirt 1 transcriptional control is critical to the prevention of MODS that is linked to the immune system and insulin resistance. In the developing world bacterial lipopolysaccharides a critical repressor of Sirt 1 is now involved with NAFLD and various organ diseases relevant to tissue accumulation of xenobiotics from various environments with relevance to MODS and the global chronic disease epidemic.
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The anti-aging gene Sirtuin 1 has now major relevance to genetics and the fields of pharmacology, toxicology, neurosci¬ence, immunology, biochemistry and cell/molecular biology. Advances in anti-aging therapy are now essential to prevent mitochondrial apoptosis to promote longevity with the pre¬vention of accelerated ageing. Calorie restriction that main¬tains the anti-aging gens changes the core body temperature and promotes species longevity. Stress and calorie consump¬tion are sensitive to Sirt 1 function with relevance heat shock protein 70 metabolism and mitochondrial biogenesis. Sirt 1 regulation of the circadian rhythm mediates melatonin effects on core body temperature regulation and immune responses. Diet and fat are essential factors that determine species lon¬gevity with relevance to heat shock gene regulation and mi¬tochondrial disease in animals and man. Strenuous exercise to activate the cellular heat shock gene in animals and man should be carefully controlled to prevent magnesium deficien¬cy with relevance to immune disorders and mitophagy.
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In the developing world food and nutrition guidelines with relevance to nutrition and metabolism are required to reduce elevated cholesterol levels with relevance to diabetes, Parkinson’s disease and Alzheimer’s disease. In diabetes and neurodegenerative diseases global non alcoholic fatty liver disease (NAFLD) has become of major concern with the reduced hepatic metabolism of toxic compounds that increase with age to milligrams quantities of bacterial lipopolysaccharides (LPS), mycotoxins and xenobiotics that induce neuron death. The increased brain content of these toxic compounds completely inactivate drug therapy with increased repetitive drug exposure to neurons and synpases. In the global diabetes epidemic diabetes is expected to double by the year 2050 in the developing world and diets that reverse or stabilize mitochondrial apoptosis have become relevant to synaptic plasticity and to prevent neuronal death. These toxic compounds determine the survival of various species with relevance to greater toxicity to neurons and their synapses in diabetes when compared to toxic amyloid beta oligomers and alpha synuclein oligomers in Parkinson’s disease and Alzheimer’s disease .
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p class="jfr-body"> Food and nutrition guidelines for the handling and processing of fresh fruit, bread, and vegetables are essential and fresh produce may require cold preservation procedures to prevent minimal bacterial and fungi contamination of food. Bacterial lipopolysaccharides (LPS) corrupt lipoprotein and amyloid beta (Aβ) metabolism in diabetes, Alzheimer’s disease (AD) and various neurological diseases. In the developing world the increased plasma LPS levels induce non-alcoholic fatty liver diseases and interfere with albumin and Aβ interactions with spontaneous Aβ oligomer formation in the cerebrospinal fluid and brain that leads to neuron apoptosis by inactivation of Starling’s equation that is responsible for the maintenance of hydrostatic and oncotic pressure with relevance to fluid balance. In the developing world increased levels of LPS, mycotoxin and xenobiotics lead to irreversible neurological diseases by inhibition of Starling’s equation for maintenance of oncotic/osmotic pressure that lead to neuron senescence or apoptosis. In the developed world nutrigenomic diets are required that prevent Sirtuin 1 gene repression and maintain neuron survival that links the brain and peripheral hepatic monomer Aβ metabolism. The maintenance of blood-cerebrospinal fluid capillary transport of albumin and monomer Aβ is relevant to stabilization of neurons not only in Alzheimer’s disease but also in Type 3 diabetes and various neurological diseases. Healthy diets reverse the inhibition of brain to peripheral Aβ transport that is sensitive to Starling’s equation for regulation of central nervous system hydrostatic and oncotic pressure with the prevention of diabetes, various neurological diseases and Alzheimer’s disease. </p
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Healthy aging and longevity in humans are modulated by a lucky combination of genetic and non-genetic factors. Family studies demonstrated that about 25 % of the variation in human longevity is due to genetic factors. The search for genetic and molecular basis of aging has led to the identification of genes correlated with the maintenance of the cell and of its basic metabolism as the main genetic factors affecting the individual variation of the aging phenotype. In addition, studies on calorie restriction and on the variability of genes associated with nutrient-sensing signaling, have shown that ipocaloric diet and/or a genetically efficient metabolism of nutrients, can modulate lifespan by promoting an efficient maintenance of the cell and of the organism. Recently, epigenetic studies have shown that epigenetic modifications, modulated by both genetic background and lifestyle, are very sensitive to the aging process and can either be a biomarker of the quality of aging or influence the rate and the quality of aging. On the whole, current studies are showing that interventions modulating the interaction between genetic background and environment is essential to determine the individual chance to attain longevity.