Association of sleep duration with apolipoproteins and the apolipoprotein B/A1 ratio: the China health and nutrition survey

Abstract

BackgroundShort sleep duration has been related to established cardiovascular risk factors, likely obesity, diabetes, hypertension and dyslipidaemia. However, to the best of our knowledge, the associations between sleep duration and apolipoprotein concentrations and their ratios have not been investigated to date. This study aimed to explore the independent relationship of sleep duration with apolipoprotein (apo) A1, apoB and the apoB/apoA1 ratio in a Chinese adult population.MethodsData from 7381 participants, aged 18 to 75 years, from the National Health and Nutrition Survey 2009 were analysed in this cross-sectional study. Participants were divided into 3 categories according to sleep duration: ≤6, 7–8, and ≥9 h. Logistic regression analysis with odds ratios was employed to assess the association between sleep duration and apo profile.ResultsUsing 7–8 h of sleep as a reference, short sleep duration was associated with significantly increased odds of elevated apoB (OR =1.75, 95% CI 1.12–2.72), whereas long sleep duration was correlated with a decreased (but not statistically significant) risk for elevated apoB (OR =0.86, 95% CI 0.54–1.38) among females after controlling for covariates. Among males, long sleep duration was only marginally related to decreased odds ratios for elevated apoB/apoA1 ratio after adjustment for covariates (OR =0.78, 95% CI 0.6–0.99).ConclusionsThese results indicate that short sleep duration is strongly associated with an increased risk of elevated apoB levels in women and that long sleep duration is correlated with decreased apoB/apoA1 levels in men. Sleep hygiene management could serve to treat and prevent cardiovascular diseases by altering unfavourable apo profile.

Blood signatures for second stage Human African Trypanosomiasis: A transcriptomic approach.

“…Furthermore genes associated with gamma-aminobutyric acid (GABRA2, GABRB) have been implicated in sleep disorders [39] including ApoB [40]. IL-10 which has been previously observed upregulated in the CSF of T. b. rhodesiense patients [41,42] was indeed more expressed in the CSF (log2FC 3.1) in addition to the other cytokines including IL12, IL17RD, IL20RA, IL21R, IL36B, IL32.…”

Are we close to defining a metabolomic signature of human obesity? A systematic review of metabolomics studies

“…According to the type of approach reported on the studies, we have divided the results into four blocks. The first block includes studies designed to determine the metabolic signature of obesity; 15 of which used an untargeted approach (Fattuoni et al 2018 ; Ruebel et al 2019 ; Houttu et al 2018 ; Sorrow et al 2019 ; Butte et al 2015 ; Kim et al 2010b ; Xie et al 2014 ; Hanzu et al 2014 ; Zhao et al 2016a , b ; Foerster et al 2015 ; Bagheri, et al 2019 , Cirulli et al 2019 , Yu et al 2018 , Marco-Ramell et al 2018 , Piening et al 2018 ), 14 used targeted metabolite profiling (Wahl et al 2012 ; Gawlik et al 2016 ; Newgard et al 2009 ; Baker et al 2015 ; Kraus et al 2016 ; Feldman et al 2019 ; Maltais-Payette et al 2018 ; Carayol et al 2017 ; Bagheri et al 2018 ; Wang et al 2018 ; Ho et al 2016 ; Haufe et al 2016 ; Stroeve et al 2016 ; Tulipani et al 2016a , b ), and one designed the metabolomics study using a combination of both approaches (Cho et al 2017 ) (Table 1 ). The second block includes five studies focused on studying the differential responses of obese and non-obese subjects to dietary challenges (Table 2 ) (Badoud et al 2015b ; Baker et al 2015 ; Geidenstam et al 2014 ; Bak et al 2018 ).…”

“…The increase, or decrease during weight loss, of BCAAs, reflect the status of the protein breakdown, which is a consequence of IR, thus pointing towards to metabolic complications. In fact, the higher concentrations of glutamate observed in six studies (Butte et al 2015 ; Newgard et al 2009 ; Yu et al 2018 ; Maltais-Payette et al 2018 ; Wang et al 2018 ; Carayol et al 2017 ) might be linked to the BCAAs alterations, since such an AA is produced as the first step of BCAAs catabolism (Newgard 2017 ).…”

Blood signatures for second stage human African trypanosomiasis: a transcriptomic approach

“…Genes within these clusters including ADCY2 and AKAP have been associated with bipolar disorder and schizophrenia [37,38]. Furthermore genes associated with gamma-aminobutyric acid (GABRA2, GABRB) have been implicated in sleep disorders [39] including ApoB [40]. IL-10 which has been previously observed up-regulated in the CSF of T. b. rhodesiense patients [41,42] was indeed more expressed in the CSF (log2FC 3.1) in addition to the other cytokines including IL12, IL17RD, IL20RA, IL21R, IL36B, IL32.…”