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Links between Immunologic Memory and Metabolic Cycling.
Cottam MA, Itani HA, Beasley AA, Hasty AH
(2018) J Immunol 200: 3681-3689
MeSH Terms: Adaptive Immunity, Animals, Body Weight, Humans, Hypertension, Immunity, Innate, Immunologic Memory, Metabolic Diseases
Show Abstract · Added March 26, 2019
Treatments for metabolic diseases, such as diet and therapeutics, often provide short-term therapy for metabolic stressors, but relapse is common. Repeated bouts of exposure to, and relief from, metabolic stimuli results in a phenomenon we call "metabolic cycling." Recent human and rodent data suggest metabolic cycling promotes an exaggerated response and ultimately worsened metabolic health. This is particularly evident with cycling of body weight and hypertension. The innate and adaptive immune systems have a profound impact on development of metabolic disease, and current data suggest that immunologic memory may partially explain this association, especially in the context of metabolic cycling. In this Brief Review, we highlight recent work in this field and discuss potential immunologic mechanisms for worsened disease prognosis in individuals who experience metabolic cycling.
Copyright © 2018 by The American Association of Immunologists, Inc.
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8 MeSH Terms
Macrophage-Targeted Therapeutics for Metabolic Disease.
Peterson KR, Cottam MA, Kennedy AJ, Hasty AH
(2018) Trends Pharmacol Sci 39: 536-546
MeSH Terms: Drug Delivery Systems, Gene Expression, Humans, Macrophages, Metabolic Diseases, Molecular Targeted Therapy, Pharmaceutical Preparations
Show Abstract · Added March 26, 2019
Macrophages are cells of the innate immune system that are resident in all tissues, including metabolic organs such as the liver and adipose tissue (AT). Because of their phenotypic flexibility, they play beneficial roles in tissue homeostasis, but they also contribute to the progression of metabolic disease. Thus, they are ideal therapeutic targets for diseases such as insulin resistance (IR), nonalcoholic fatty liver disease (NAFLD), and atherosclerosis. Recently, discoveries in the area of drug delivery have facilitated phenotype-specific targeting of macrophages. In this review we discuss advances in potential therapeutics for metabolic diseases via macrophage-specific delivery. We highlight micro- and nanoparticles, liposomes, and oligopeptide complexes, and how they can be used to alter macrophage phenotype for a more metabolically favorable tissue environment.
Published by Elsevier Ltd.
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MeSH Terms
DOHaD at the intersection of maternal immune activation and maternal metabolic stress: a scoping review.
Goldstein JA, Norris SA, Aronoff DM
(2017) J Dev Orig Health Dis 8: 273-283
MeSH Terms: Animals, Case-Control Studies, Cross-Sectional Studies, Female, Humans, Infant, Low Birth Weight, Metabolic Diseases, Pregnancy, Pregnancy Complications, Premature Birth, Prospective Studies, Randomized Controlled Trials as Topic, Retrospective Studies, Stress, Physiological
Show Abstract · Added June 2, 2017
The prenatal environment is now recognized as a key driver of non-communicable disease risk later in life. Within the developmental origins of health and disease (DOHaD) paradigm, studies are increasingly identifying links between maternal morbidity during pregnancy and disease later in life for offspring. Nutrient restriction, metabolic disorders during gestation, such as diabetes or obesity, and maternal immune activation provoked by infection have been linked to adverse health outcomes for offspring later in life. These factors frequently co-occur, but the potential for compounding effects of multiple morbidities on DOHaD-related outcomes has not received adequate attention. This is of particular importance in low- or middle-income countries (LMICs), which have ongoing high rates of infectious diseases and are now experiencing transitions from undernutrition to excess adiposity. The purpose of this scoping review is to summarize studies examining the effect and interaction of co-occurring metabolic or nutritional stressors and infectious diseases during gestation on DOHaD-related health outcomes. We identified nine studies in humans - four performed in the United States and five in LMICs. The most common outcome, also in seven of nine studies, was premature birth or low birth weight. We identified nine animal studies, six in mice, two in rats and one in sheep. The interaction between metabolic/nutritional exposures and infectious exposures had varying effects including synergism, inhibition and independent actions. No human studies were specifically designed to assess the interaction of metabolic/nutritional exposures and infectious diseases. Future studies of neonatal outcomes should measure these exposures and explicitly examine their concerted effect.
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14 MeSH Terms
The metabolic and cardiovascular consequences of obesity in persons with HIV on long-term antiretroviral therapy.
Koethe JR, Grome H, Jenkins CA, Kalams SA, Sterling TR
(2016) AIDS 30: 83-91
MeSH Terms: Adult, Anti-Retroviral Agents, Benzoxazines, Cardiovascular Diseases, Cohort Studies, Emtricitabine, Female, HIV Infections, Humans, Male, Metabolic Diseases, Middle Aged, Obesity, Risk Assessment, Tenofovir
Show Abstract · Added February 17, 2016
OBJECTIVE - This study assessed the effect of obesity on metabolic and cardiovascular disease risk factors in HIV-infected adults on antiretroviral therapy with sustained virologic suppression.
DESIGN - Observational, comparative cohort study with three group-matched arms: 35 nonobese and 35 obese HIV-infected persons on efavirenz, tenofovir and emtricitabine with plasma HIV-1 RNA  less than  50  copies/ml for more than 2 years, and 30 obese HIV-uninfected controls. Patients did not have diabetes or known cardiovascular disease.
METHODS - We compared glucose tolerance, serum lipids, brachial artery flow-mediated dilation, carotid intima-media thickness, and soluble inflammatory and vascular adhesion markers between nonobese and obese HIV-infected patients, and between obese HIV-infected and HIV-uninfected patients, using Wilcoxon rank-sum tests and multivariate linear regression.
RESULTS - The cohort was 52% men and 48% nonwhite. Nonobese and obese HIV-infected patients did not differ by clinical or demographic characteristics. Obese HIV-uninfected controls were younger than obese HIV-infected patients and less likely to smoke (P < 0.03 for both). Among HIV-infected patients, obesity was associated with greater insulin release, lower insulin sensitivity, and higher serum high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 1 levels (P < 0.001), but similar lipid profiles, sCD14, sCD163, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1, and carotid intima-media thickness and flow mediated dilation. In contrast, Obese HIV-infected patients had adverse lipid changes, and greater circulating intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and sCD14, compared with obese HIV-uninfected controls after adjusting for age and other factors.
CONCLUSION - Obesity impairs glucose metabolism and contributes to circulating high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 1 levels, but has few additive effects on dyslipidemia and endothelial activation, in Obese HIV-infected adults on long-term antiretroviral therapy.
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15 MeSH Terms
A decade of progress in adipose tissue macrophage biology.
Hill AA, Reid Bolus W, Hasty AH
(2014) Immunol Rev 262: 134-52
MeSH Terms: Adipose Tissue, Animals, Body Weight, Cell Movement, Cytokines, Homeostasis, Humans, Inflammation Mediators, Macrophages, Metabolic Diseases, Organ Specificity, Panniculitis, Phenotype, Signal Transduction
Show Abstract · Added January 21, 2015
One decade has passed since seminal publications described macrophage infiltration into adipose tissue (AT) as a key contributor to inflammation and obesity-related insulin resistance. Currently, a PubMed search for 'adipose tissue inflammation' reveals over 3500 entries since these original reports. We now know that resident macrophages in lean AT are alternatively activated, M2-like, and play a role in AT homeostasis. In contrast, the macrophages in obese AT are dramatically increased in number and are predominantly classically activated, M1-like, and promote inflammation and insulin resistance. Mediators of AT macrophage (ATM) phenotype include adipokines and fatty acids secreted from adipocytes as well as cytokines secreted from other immune cells in AT. There are several mechanisms that could explain the large increase in ATMs in obesity. These include recruitment-dependent mechanisms such as adipocyte death, chemokine release, and lipolysis of fatty acids. Newer evidence also points to recruitment-independent mechanisms such as impaired apoptosis, increased proliferation, and decreased egress. Although less is known about the homeostatic function of M2-like resident ATMs, recent evidence suggests roles in AT expansion, thermoregulation, antigen presentation, and iron homeostasis. The field of immunometabolism has come a long way in the past decade, and many exciting new discoveries are bound to be made in the coming years that will expand our understanding of how AT stands at the junction of immune and metabolic co-regulation.
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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14 MeSH Terms
Approach to assessing determinants of glucose homeostasis in the conscious mouse.
Hughey CC, Wasserman DH, Lee-Young RS, Lantier L
(2014) Mamm Genome 25: 522-38
MeSH Terms: Animals, Consciousness, Energy Metabolism, Glucose, Homeostasis, Insulin Resistance, Metabolic Diseases, Metabolome, Metabolomics, Mice, Mice, Transgenic, Models, Animal, Mutation, Phenotype
Show Abstract · Added July 31, 2014
Obesity and type 2 diabetes lessen the quality of life of those afflicted and place considerable burden on the healthcare system. Furthermore, the detrimental impact of these pathologies is expected to persist or even worsen. Diabetes is characterized by impaired insulin action and glucose homeostasis. This has led to a rapid increase in the number of mouse models of metabolic disease being used in the basic sciences to assist in facilitating a greater understanding of the metabolic dysregulation associated with obesity and diabetes, the identification of therapeutic targets, and the discovery of effective treatments. This review briefly describes the most frequently utilized models of metabolic disease. A presentation of standard methods and technologies on the horizon for assessing metabolic phenotypes in mice, with particular emphasis on glucose handling and energy balance, is provided. The article also addresses issues related to study design, selection and execution of metabolic tests of glucose metabolism, the presentation of data, and interpretation of results.
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14 MeSH Terms
β-Aminoisobutyric acid induces browning of white fat and hepatic β-oxidation and is inversely correlated with cardiometabolic risk factors.
Roberts LD, Boström P, O'Sullivan JF, Schinzel RT, Lewis GD, Dejam A, Lee YK, Palma MJ, Calhoun S, Georgiadi A, Chen MH, Ramachandran VS, Larson MG, Bouchard C, Rankinen T, Souza AL, Clish CB, Wang TJ, Estall JL, Soukas AA, Cowan CA, Spiegelman BM, Gerszten RE
(2014) Cell Metab 19: 96-108
MeSH Terms: Adipocytes, Brown, Adipocytes, White, Adipose Tissue, Brown, Adipose Tissue, White, Aminoisobutyric Acids, Animals, Cardiovascular Diseases, Cell Differentiation, Exercise, Gene Expression Regulation, Glucose Tolerance Test, Humans, Induced Pluripotent Stem Cells, Liver, Metabolic Diseases, Mice, Organ Specificity, Oxidation-Reduction, PPAR alpha, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Phenotype, Physical Conditioning, Animal, Risk Factors, Transcription Factors, Transcription, Genetic, Weight Gain
Show Abstract · Added February 28, 2014
The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases.
Copyright © 2014 Elsevier Inc. All rights reserved.
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26 MeSH Terms
Cytochromes p450: roles in diseases.
Pikuleva IA, Waterman MR
(2013) J Biol Chem 288: 17091-8
MeSH Terms: Animals, Cholecalciferol, Cytochrome P-450 Enzyme System, Eicosanoids, Humans, Metabolic Diseases, Mutation, Steroids
Show Abstract · Added March 7, 2014
The cytochrome P450 superfamily consists of a large number of heme-containing monooxygenases. Many human P450s metabolize drugs used to treat human diseases. Others are necessary for synthesis of endogenous compounds essential for human physiology. In some instances, alterations in specific P450s affect the biological processes that they mediate and lead to a disease. In this minireview, we describe medically significant human P450s (from families 2, 4, 7, 11, 17, 19, 21, 24, 27, 46, and 51) and the diseases associated with these P450s.
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8 MeSH Terms
Mitochondrial genomics and antiretroviral therapy-associated metabolic complications in HIV-infected Black South Africans: a pilot study.
Sinxadi PZ, Dave JA, Samuels DC, Heckmann JM, Maartens G, Levitt NS, Wester CW, Haas DW, Hulgan T
(2013) AIDS Res Hum Retroviruses 29: 1031-9
MeSH Terms: Adult, African Continental Ancestry Group, Anti-HIV Agents, Cross-Sectional Studies, DNA, Mitochondrial, Female, Genetic Predisposition to Disease, Genetic Variation, Genome, Mitochondrial, HIV Infections, HIV-Associated Lipodystrophy Syndrome, Humans, Hypertriglyceridemia, Male, Metabolic Diseases, Pilot Projects, Polyneuropathies, South Africa
Show Abstract · Added December 12, 2013
Studies suggest that mitochondrial DNA (mtDNA) haplogroups are associated with antiretroviral therapy (ART)-related metabolic complications and distal sensory polyneuropathy (DSP), but there have been few studies in persons of African descent. We explored such associations in South African adults. Clinical and laboratory data and DNA specimens from a cross-sectional study were used. Sequencing and Phylotree determined African mtDNA subhaplogroups. Wilcoxon and regression analyses determined associations between mtDNA subhaplogroups and ART-related complications. The 171 participants represented six major haplogroups: L0 (n=78), L1 (n=3), L2 (n=30), L3 (n=53), L4 (n=1), and L5 (n=6). Analyses were restricted to 161 participants representing L0, L2, and L3: 78% were female; the median age was 36 years. All had been exposed to thymidine analogues, 42% were on lopinavir/ritonavir (lopinavir/r), and 58% were on either efavirenz or nevirapine. Median (IQR) ART duration was 22 (14-36) months. Median fasting triglycerides were 1.60 (1.13-1.75) and 1.04 (0.83-1.45) mmol/liter among L3e1 (n=22) and other subhaplogroups, respectively (p=0.003). Subhaplogroup L3e1 [adjusted OR (aOR) 3.16 (95% CI: 1.11-8.96); p=0.03] and exposure to lopinavir/r [aOR 2.98 (95% CI: 1.02-8.96); p=0.05] were independently associated with hypertriglyceridemia, after adjusting for age, sex, and ART duration. There were no significant associations between mtDNA haplogroups and cholesterol, dysglycemia, hyperlactatemia, or lipoatrophy, or DSP. Subhaplogroup L3e1 and lopinavir/r exposure were independently associated with hypertriglyceridemia in black South Africans on ART. This is the first report to link an African mtDNA variant with hypertriglyceridemia. If replicated, these findings may provide new insights into host factors affecting metabolic complications.
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18 MeSH Terms
Evaluation of the metabochip genotyping array in African Americans and implications for fine mapping of GWAS-identified loci: the PAGE study.
Buyske S, Wu Y, Carty CL, Cheng I, Assimes TL, Dumitrescu L, Hindorff LA, Mitchell S, Ambite JL, Boerwinkle E, Buzkova P, Carlson CS, Cochran B, Duggan D, Eaton CB, Fesinmeyer MD, Franceschini N, Haessler J, Jenny N, Kang HM, Kooperberg C, Lin Y, Le Marchand L, Matise TC, Robinson JG, Rodriguez C, Schumacher FR, Voight BF, Young A, Manolio TA, Mohlke KL, Haiman CA, Peters U, Crawford DC, North KE
(2012) PLoS One 7: e35651
MeSH Terms: African Americans, Cardiovascular Diseases, Cholesterol Ester Transfer Proteins, Cholesterol, HDL, Cholesterol, LDL, Chromosomes, Human, Cohort Studies, Gene Frequency, Genome-Wide Association Study, Genotype, Humans, Metabolic Diseases, Polymorphism, Single Nucleotide, Quantitative Trait Loci
Show Abstract · Added December 10, 2013
The Metabochip is a custom genotyping array designed for replication and fine mapping of metabolic, cardiovascular, and anthropometric trait loci and includes low frequency variation content identified from the 1000 Genomes Project. It has 196,725 SNPs concentrated in 257 genomic regions. We evaluated the Metabochip in 5,863 African Americans; 89% of all SNPs passed rigorous quality control with a call rate of 99.9%. Two examples illustrate the value of fine mapping with the Metabochip in African-ancestry populations. At CELSR2/PSRC1/SORT1, we found the strongest associated SNP for LDL-C to be rs12740374 (p = 3.5 × 10(-11)), a SNP indistinguishable from multiple SNPs in European ancestry samples due to high correlation. Its distinct signal supports functional studies elsewhere suggesting a causal role in LDL-C. At CETP we found rs17231520, with risk allele frequency 0.07 in African Americans, to be associated with HDL-C (p = 7.2 × 10(-36)). This variant is very rare in Europeans and not tagged in common GWAS arrays, but was identified as associated with HDL-C in African Americans in a single-gene study. Our results, one narrowing the risk interval and the other revealing an associated variant not found in Europeans, demonstrate the advantages of high-density genotyping of common and rare variation for fine mapping of trait loci in African American samples.
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14 MeSH Terms