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Abstract Background A persistent redox state and excessive reactive species involved in carbohydrate and lipid metabolism lead to oxidative damage in the liver, however, how fasting plasma concentrations of lipids and glucose are associated with fasting blood levels of alanine transaminase (ALT) and aspartate transaminase (AST) remains to be evaluated in large-scale population. Methods A cross-sectional study with 182,971 residents aged 18 to 92 years; multidimensional stratified analyses including quantile linear regression analysis and sex stratification were adopted to improve the quality of the evidence. Results The associations between the concentrations of non-HDL-C and triglyceride and ALT levels were positive, stronger in males in each quantile of ALT levels and the coefficients expanded with increasing ALT levels at slopes of 3.610 and 5.678 in males and 2.977 and 5.165 in females, respectively. The associations between the HDL-C concentrations and ALT levels were negative, also stronger in males in each quantile and the coefficients expanded with increasing ALT levels at slopes of -7.839 in females and − 5.797 in males. The associations between glucose concentrations and ALT levels were positive, but stronger in females in each quantile and the coefficients expanded with increasing ALT levels at slopes of 1.736 in males and 2.177 in females, respectively. Similar pattern consist of relatively weaker coefficients and slops were observed between concentrations of non-HDL-C, triglyceride and glucose and AST levels. The associations between albumin concentration and concentrations of blood lipids and glucose were relatively steady across all quantiles. Conclusions The dose dependent effect between blood concentrations of lipids and glucose and liver function changes suggests that excessive carbohydrate and lipid metabolism may cause subclinical liver damage. Long term sustained primary and secondary inflammatory factors produced in the liver might be transmitted to adjacent organs, such as the heart, kidneys, and lungs, to cause and/or exacerbate pathological changes in these visceral organs.

Background: A persistent redox state and excessive reactive species involved in carbohydrate and lipid metabolism lead to oxidative damage in the liver, however, how fasting plasma concentrations of lipids and glucose are associated with fasting blood levels of alanine transaminase (ALT) and aspartate transaminase (AST) remains to be evaluated in large-scale population. Methods: A cross-sectional study with 182,971 residents aged 18 to 92 years; multidimensional stratified analyses including quantile linear regression analysis and sex stratification were adopted to improve the quality of the evidence. Results: The associations between the concentrations of non-HDL-C and triglyceride and ALT levels were positive, stronger in males in each quantile of ALT levels and the coefficients expanded with increasing ALT levels at slopes of 3.610 and 5.678 in males and 2.977 and 5.165 in females, respectively. The associations between the HDL-C concentrations and ALT levels were negative, also stronger in males in each quantile and the coefficients expanded with increasing ALT levels at slopes of -7.839 in females and − 5.797 in males. The associations between glucose concentrations and ALT levels were positive, but stronger in females in each quantile and the coefficients expanded with increasing ALT levels at slopes of 1.736 in males and 2.177 in females, respectively. Similar pattern consist of relatively weaker coefficients and slops were observed between concentrations of non-HDL-C, triglyceride and glucose and AST levels. The associations between albumin concentration and concentrations of blood lipids and glucose were relatively steady across all quantiles. Conclusions: The dose dependent effect between blood concentrations of lipids and glucose and liver function changes suggests that excessive carbohydrate and lipid metabolism may cause subclinical liver damage. Long term sustained primary and secondary inflammatory factors produced in the liver might be transmitted to adjacent organs, such as the heart, kidneys, and lungs, to cause and/or exacerbate pathological changes in these visceral organs. [ABSTRACT FROM AUTHOR]

Abstract: Background: OSAS, a frequently neglected, yet frequent comorbidity in T2DM, is associated with obesity, metabolic syndrome and central fat. OSAS is better documented in males, and this study explored novel gender dimorphisms in T2DM. Methods: Cross-sectional study: 815 T2DM (541 males; 274 females) classified into OSAS[−] and OSAS[+] were assessed for cardiometabolic risk factors, glucose homeostasis, micro/macroangiopathies, CV risk, autoimmune thyroid disease (AITD); and GAD65 antibodies. Results: There was a gender dimorphism in glucose control (worse in females), apolipoprotein B100 (higher in females), with apoB100/apoA1 and log(TG)/HDL-C sexually dimorphic. There was also a marked gender dimorphism in GAD65 positivity, higher (+793%) in OSAS[+] females vs. males. There were clear sexual dimorphisms in macro-/microangioathies, regarding stroke, retinopathy and polyneuropathy. OSAS was not sexually dimorphic regarding age; education; and diabetes duration. There was a significant dimorphism in ethnicity. There were no gender-specific dimorphisms related to OSAS in anthropometrics, nor in hypertension, insulin sensitivity, or hyperbolic product loss rate. Conclusion: We report a series of novel OSAS-related sexual dimorphisms, concerning GAD65 auto-antibodies; polyneuropathy; atherogenic dyslipidemia [all increased in females]; diabetic retinopathy; North-Caucasian ethnicity; metabolic control; and TIA/stroke prevalence [all lower in females]. These findings raise challenging questions regarding the reciprocal pathophysiology between obstructive sleep disorders and cardiometabolic risk in T2DM. [Copyright &y& Elsevier]

Abstract: This study used the Purdie assay, a new assay, to quantify the levels of omega-3 (ω-3) and omega-6 (ω-6) polyunsaturated fatty acids (PUFAs) in mol/L and the ratio of ω-6:ω-3 in Total cholesterol (TC), high-density lipoprotein cholesterol, (HDL-C) and low-density lipoprotein cholesterol (LDL-C) (referred to throughout as “non-HDL-C” in this study) fractions in 35 samples of human serum and also assessed the influence of gender and cholesterol types on levels of the analyzed PUFAs. Three principal components explained 89% of the total variance based on the variables measured. The ratio of ω-6:ω-3 PUFAs was significantly influenced by the type of cholesterol (F=10.84, df=2, 99, P =< 0.001) but not gender or interaction between gender and type of cholesterol, while the total PUFAs and the levels of ω-3 and ω-6 PUFAs were significantly influenced by gender, but age did not have a significant effect on the levels for total PUFAs. The findings of this study imply that, for males, more focus should be on the ratios of ω-6:ω-3 PUFAs in the non-HDL-C fraction and that the use of the ω-6:ω-3 ratio of PUFAs in serum is a better predictor of coronary heart disease than estimating LDL-C. [Copyright &y& Elsevier]

Understanding how blood lipid levels change with age in the general population is a precondition to defining dyslipidemia. To explore age-related trends in LDL-C and non-HDL-C levels in the general population, a large-scale cross-sectional study with 49,201 males and 35,084 females was adopted. Trends of non-HDL-C and LDL-C levels were plotted against each age (18 to 85 years old, one-year increments); the trends, as well as the influence of confounding factors on the trends, were validated and adjusted by linear regression modeling. The trajectory of LDL-C and non-HDL-C levels by age displayed a nonlinear correlation trend. Further multivariate linear regression modeling that incorporated sex-specific age phases showed that age was positively associated with LDL-C and non-HDL-C levels, with coefficients of 0.018 and 0.031, respectively, in females aged ≥18 to ≤56 years and negatively associated with LDL-C and non-HDL-C levels, with coefficients of -0·013 and -0.015, respectively, in females aged ≥57 years. The LDL-C and non-HDL-C levels increased with age in males ≥18 to ≤33 years of age, with coefficients of 0.025 and 0.053, respectively; the lipid levels plateaued at ≥34 to ≤56 years of age and subsequently decreased in those ≥57 years of age, with coefficients of -0.008 and -0.018, respectively. In contrast, pooled analyses without age stratification concealed these details. In conclusion, fluctuating increasing and decreasing lipid levels occurred with phases of aging in both sexes. Well-grounded age stratification is necessary to improve lipid-related pathophysiological studies., Competing Interests: Conflict of interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (copyright: © 2020 Zhang et al.)

Background: Clinical practice guidelines (CPGs) provide many recommendations for hyperlipidemia management, but some of them are still debatable., Methods: We applied the six-domain Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument to evaluate the quality of guidelines with lipid management recommendations for coronary heart disease (CHD), including dyslipidemia and CHD guidelines published from 2009 to 2019. Meanwhile, we synthesized and compared major recommendations and present the consistency and controversy in current dyslipidemia management., Results: Among 19 guidelines included, ten guidelines ("strongly recommended" with AGREE scores 61-94%) performed better than the other nine (38-65% as "recommended with some modification") For blood lipid tests, most CHD guidelines simply required fasting sample while dyslipidemia guidelines preferred non-fasting sample except in high triglycerides state. Most guidelines consistently chose low-density lipoprotein cholesterol (LDL-C) as the primary lipid-lowering target (LLT), while non-high-density lipoprotein cholesterol (non-HDL-C) and apolipoprotein B were mainly selected as secondary LLTs. The specific goals of LDL-C lowering were either to lower than 70 mg/dL or with at least 50% reduction. All guidelines recommended high intensity or maximally tolerable doses of statins, while ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors were recommended as second-line therapy., Conclusions: The general quality of guidelines for lipid management is satisfactory. Consensus has been reached on the specific goal of lipid reduction and the intensity of statins therapy. Further research is needed to validate the application of non-fasting sample and non-HDL-C target, as well as the efficacy and safety of ezetimibe and PCSK9 inhibitors., Competing Interests: Conflicts of Interest: The authors have no conflicts of interest to declare.