Circadian rhythms in liver metabolism and disease.
ARC; arcuate nucleus; BMAL1; brain and muscle ARNT-like 1; CAR; cholesterol 7alpha-hydroxylase; circadian locomotor output cycles kaput; Circadian rhythm; CLOCK; constitutive androstane receptor; CRY; cryptochrome; CYP7A1; CYPs; cytochrome P450 enzymes; D-site binding protein; DBP; E-box; emergency medical technician; EMT; enhance box; FAA; familial advanced sleep-phase syndrome; farnesoid-X receptor; FASPS; FEO; food anticipatory activity; food entrainable oscillator; forkhead box O3; FOXO3; FXR; G protein-coupled bile acid receptor; glucose transporter 2; GLUT2; HDAC3; hepatic leukemia factor; HIP; histone deacetylase 3; HLF; hypoxia inducing protein; LDL; Liver; liver receptor homolog 1; low-density lipoprotein; LRH1; Metabolic syndrome; NAD+; nicotinamide adenine dinucleotide; PER; period; retinohypothalamic tract; retinoid-related orphan receptor alpha; RHT; ROR-response element; RORalpha; RORE; SCN; SHP; SIRT1; sirtuin 1; small heterodimer partner; suprachiasmatic nucleus; TEF; TGR5; thyrotroph embryonic factor; transcriptional translational feedback loop; TTFL; Type 2 diabetes
Mounting research evidence demonstrates a significant negative impact of circadian disruption on human health. Shift work, chronic jet lag and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.
Ferrell Jessica M; Chiang John Y L
Acta pharmaceutica Sinica. B
2015
2015-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.apsb.2015.01.003" target="_blank" rel="noreferrer noopener">10.1016/j.apsb.2015.01.003</a>
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation
potassium channels; exercise; Physiology; Cardiovascular System & Cardiology; blood flow; activation; smooth-muscle-cells; heart; adenosine; adenosine triphosphate-dependent; arterioles; calcium-activated potassium channels; cardiovascular-disease mortality; coronary reactive hyperemia; myocardial reactive hyperemia; Ossabaw miniature swine; sensitive potassium channels; type 2 diabetes; voltage-activated potassium channels
Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol 298: H1182-H1189, 2010. First published January 29, 2010; doi: 10.1152/ajpheart.00888.2009.-This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K+ channels to coronary reactive hyperemia. Ca2+-activated (BKCa), voltage-activated (K-V), and ATP-dependent (K-ATP) K+ channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BKCa (penitrem A; 10 mu g/kg iv), K-V (4-aminopyridine; 0.3 mg/kg iv) and K-ATP (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced similar to 30% compared with lean swine. Inhibition of BKCa channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of KV channels significantly reduced the repayment of flow debt (similar to 25%) in both lean and metabolic syndrome swine. Additional blockade of K-ATP channels further diminished (similar to 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K+ channels to reactive hyperemia.
Borbouse L; Dick G M; Payne G A; Berwick Z C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
American Journal of Physiology-Heart and Circulatory Physiology
2010
2010-04
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2009</a>
Targeting Mitochondrial Dna To Reduce Consequences Of Oxidative Stress: Role In The Prevention Of The Diabetic Cardiomyopathy
arrhythmias; Cardiovascular System & Cardiology; Coronary circulation; Coronary microcirculation; heart failure; Mitochondrial energetics; oxidative stress; Type 2 Diabetes
Guarini G; Kolz C L; Pung Y F; Ohanyan V A; Yin L Y; Bratz I N; Marzilli M; Chilian W M
Circulation
2011
2011-11
Journal Article or Conference Abstract Publication
n/a
Temporal Dynamics of High-Density Lipoprotein Proteome in Diet-Controlled Subjects with Type 2 Diabetes.
apolipoproteins; HDL dysfunction; heavy water; proteomics; type 2 diabetes
We examined the effect of mild hyperglycemia on high-density lipoprotein (HDL) metabolism and kinetics in diet-controlled subjects with type 2 diabetes (T2D). (2)H2O-labeling coupled with mass spectrometry was applied to quantify HDL cholesterol turnover and HDL proteome dynamics in subjects with T2D (n = 9) and age- and BMI-matched healthy controls (n = 8). The activities of lecithin-cholesterol acyltransferase (LCAT), cholesterol ester transfer protein (CETP), and the proinflammatory index of HDL were quantified. Plasma adiponectin levels were reduced in subjects with T2D, which was directly associated with suppressed ABCA1-dependent cholesterol efflux capacity of HDL. The fractional catabolic rates of HDL cholesterol, apolipoprotein A-II (ApoA-II), ApoJ, ApoA-IV, transthyretin, complement C3, and vitamin D-binding protein (all p < 0.05) were increased in subjects with T2D. Despite increased HDL flux of acute-phase HDL proteins, there was no change in the proinflammatory index of HDL. Although LCAT and CETP activities were not affected in subjects with T2D, LCAT was inversely associated with blood glucose and CETP was inversely associated with plasma adiponectin. The degradation rates of ApoA-II and ApoA-IV were correlated with hemoglobin A1c. In conclusion, there were in vivo impairments in HDL proteome dynamics and HDL metabolism in diet-controlled patients with T2D.
Kheniser Karim G; Osme Abdullah; Kim Chunki; Ilchenko Serguei; Kasumov Takhar; Kashyap Sangeeta R
Biomolecules
2020
2020-03-30
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.3390/biom10040520" target="_blank" rel="noreferrer noopener">10.3390/biom10040520</a>
The C1q/TNF-related proteins (CTRPS) in pathogenesis of obesity-related metabolic disorders: Focus on type 2 diabetes and cardiovascular diseases.
Obesity; Type 2 diabetes; Cardiovascular diseases; C1q/TNF-related proteins (CTRPs)
The growing evidence has been tried to explain and characterize C1q/TNF- related proteins (CTRPs) family as the potential diagnostic or therapeutic targets of obesity-related metabolic disorders such as insulin resistance, type 2 diabetes (T2D), and cardiovascular disorders. However, the underlying mechanism is still obscure. Unraveling the signaling pathways downstream of CTRP family members is of great interest and could certainly be beneficial for finding new insights into therapeutic strategies for improving metabolic abnormalities. This review focused on the role of CTRP members in the initiation and development of obesity-related metabolic disorders with a focus on T2D and cardiovascular diseases. Here we summarize and discuss the role of CTRPs in the regulation of insulin signaling, inflammatory pathways, and energy metabolism, and other signaling pathways pertinent to the pathogenesis of T2D and cardiovascular diseases. We also review available clinical studies to better elucidate the roles of these potential molecules in the initiation and development of the afore-mentioned disorders.
Shanaki M; Shabani P; Goudarzi A; Omidifar A; Bashash D; Emamgholipour S
Life Sciences
2020
2020-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.1016/j.lfs.2020.117913" target="_blank" rel="noreferrer noopener">10.1016/j.lfs.2020.117913</a>