Hepatic ATGL knockdown uncouples glucose intolerance from liver TAG accumulation.

Adipose triglyceride lipase (ATGL) is the predominant triacylglycerol (TAG) hydrolase in mammals; however, the tissue-specific effects of ATGL outside of adipose tissue have not been well characterized. Hence, we tested the contribution of hepatic ATGL on mediating glucose tolerance and insulin action. Glucose or insulin tolerance tests and insulin signaling were performed in C57BL/6 mice administered control (nongene specific shRNA) or Atgl shRNA adenoviruses. Glucose and lipid metabolism assays were conducted in primary hepatocytes isolated from mice transduced with control or Atgl shRNA adenoviruses. Knocking down hepatic ATGL completely abrogated the increase in serum insulin following either 1 or 12 wk of feeding a high-fat (HF) diet despite higher hepatic TAG content. Glucose tolerance tests demonstrated that ATGL knockdown normalized glucose tolerance in HF-diet-fed mice. The observed improvements in glucose tolerance were present despite unaltered hepatic insulin signaling and increased liver TAG. Mice with suppressed hepatic ATGL had reduced hepatic glucose production in vivo, and hepatocytes isolated from Atgl shRNA-treated mice displayed a 26% decrease in glucose production and a 38% increase in glucose oxidation compared to control cells. Taken together, these data suggest that hepatic ATGL knockdown enhances glucose tolerance by increasing hepatic glucose utilization and uncouples impairments in insulin action from hepatic TAG accumulation.

Role of Dgat2 in Glucose Uptake and Fatty Acid Metabolism in C2C12 Skeletal Myotubes.

Acyl-coenzyme A (CoA):diacylglycerol acyltransferase 2 (DGAT2) catalyzes the last stage of triacylglycerol (TAG) synthesis, a process that forms ester bonds with diacylglycerols (DAG) and fatty acyl-CoA substrates. The enzymatic role of Dgat2 has been studied in various biological species. Still, the full description of how Dgat2 channels fatty acids in skeletal myocytes and the consequence thereof in glucose uptake have yet to be well established. Therefore, this study explored the mediating role of Dgat2 in glucose uptake and fatty acid partitioning under short interfering ribonucleic acid (siRNA)-mediated Dgat2 knockdown conditions. Cells transfected with Dgat2 siRNA downregulated glucose transporter type 4 (Glut4) messenger RNA (mRNA) expression and decreased the cellular uptake of [1-14C]-labeled 2-deoxyglucose up to 24.3% (p < 0.05). Suppression of Dgat2 deteriorated insulininduced Akt phosphorylation. Dgat2 siRNA reduced [1-14C]-labeled oleic acid incorporation into TAG, but increased the level of [1-14C]-labeled free fatty acids at 3 h after initial fatty acid loading. In an experiment of chasing radioisotope-labeled fatty acids, Dgat2 suppression augmented the level of cellular free fatty acids. It decreased the level of re-esterification of free fatty acids to TAG by 67.6% during the chase period, and the remaining pulses of phospholipids and cholesteryl esters were decreased by 34.5% and 61%, respectively. Incorporating labeled fatty acids into beta-oxidation products increased in Dgat2 siRNA transfected cells without gene expression involving fatty acid oxidation. These results indicate that Dgat2 has regulatory function in glucose uptake, possibly through the reaction of TAG with endogenously released or recycled fatty acids.

Association of skeletal muscle mass and risk of hypertension in Korean adults: secondary analysis of data from the community-based prospective cohort study.

Background: Cross-sectional studies have revealed a link between low muscle mass and hypertension. However, whether the degree of muscle mass predicts hypertension risk has not been confirmed. This study aimed to verify an association between skeletal muscle mass and incident hypertension in a longitudinal follow-up of middle-aged Korean adults. Methods: The community-based prospective Korean Genome and Epidemiology Study (KoGES) data from 2,669 participants who were free of hypertension at baseline were prospectively assessed at 2-year intervals for 16 years. The participants were divided into tertiles T1-T3 of relative skeletal muscle mass (RSM) according to their baseline whole-body skeletal muscle mass measured as bioelectrical impedance. Incident hypertension was estimated using multivariate logistic regression with the Cox proportional hazard regression model. Results: Over the 16-year follow-up, the rates of incident hypertension at RSM T1, T2, and T3 were 18.7, 17.1, and 13.4% in men (P for trend = 0.0002) and 18.8, 14.7, and 12.9% in women (P for trend = 0.0007), respectively. The multivariate adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for the incidence of hypertension for men and women in T1 and T2 were 1.36 (1.11-1.67) and 1.59 (1.31-1.94), and 1.20 (0.99-1.46) and 1.70 (1.41-2.04), respectively, compared with T3 as the reference. Conclusion: A low skeletal muscle mass in middle-aged Korean men and women was significantly associated with incident hypertension in later life. Further investigation is needed to comprehend the mechanisms of this relationship and validate the findings in a large cohort.

Effects of Omega-3 Fatty Acid Supplementation on Skeletal Muscle Mass and Strength in Adults: A Systematic Review.

Previous studies have suggested that omega-3 polyunsaturated fatty acids, predominantly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have several health benefits. However, their effect on changes in skeletal muscle mass and strength has not been established, owing to differences in study designs. This systematic review aimed to investigate the recent evidence regarding the role of dietary EPA and DHA in muscle mass changes and their association with muscle strength. Databases including PubMed and Google Scholar were searched for randomized controlled trials and single-arm interventions that investigated the effects of omega-3 fatty acids on skeletal muscle mass, strength, and body composition in adults aged 18 years and older. A total of 18,521 studies were retrieved from the databases and manual searches; 21 studies were quality assessed, and the findings were summarized. Studies were categorized into 3 main categories according to the type of omega-3 fatty acid supplementation: pure compounds such as oil tablets, formulated forms with protein, leucine, and vitamin D, and ingredients added to enteral nutrition support products. Overall, the majority of the study results appeared to indicate that omega-3 fatty acids are beneficial for muscle health. However, meta-analysis was not conducted because of the heterogeneity of the study participants, evaluation method of muscle indices, and intervention periods among the studies. High-quality studies are required to validate our conclusions. However, this systematic review of the effects of EPA and DHA on skeletal muscle and body composition provides evidence that can be applied in both clinical and industrial settings.

The ability of the geriatric nutritional risk index to predict the risk of heart diseases in Korean adults: a Korean Genome and Epidemiology Study cohort.

Introduction: The predictive ability of nutritional risk index on cardiovascular outcomes in middle-aged and non-hospitalized adults has not yet been reported. This study investigated whether the Geriatric Nutritional Risk Index (GNRI), an index for assessing the risk of developing malnutrition, could predict heart disease in middle-aged Korean adults. Methods: The cohort used in this study consisted of 3,783 participants selected from 10,030 Korean adults who participated in the Ansan-Ansung cohort study as part of the Korean Genome and Epidemiology Study. The GNRI was determined based on serum albumin level, proportion of current weight, and ideal body weight. Participants were then divided into two groups: GNRI ≤98 and > 98, which corresponded to the risk of malnutrition and normal, respectively. The major outcome of this study was coronary artery disease (CAD) or congestive heart failure (CHF) during a 15-year-follow period. Results: During the follow-up period spanning 2004-2018, 136 events of heart disease occurred. Using a Kaplan-Meier analysis, event-free rates were found to be associated with 90.5% on a GNRI ≤98 and 96.6% on a GNRI >98 (p < 0.0009). GNRI ≤98 showed a 3.2-fold (hazard ratio, 3.22; 95% credit interval, 1.49-6.96; p = 0.0029) increase in the incidence of heart disease, including CAD or CHF, compared with GNRI >98, after controlling for potential confounders. Conclusion: Malnutrition risk confers a significantly increased risk for heart disease in middle-aged Koreans. Further studies with larger cohorts are needed to verify the efficacy of the GNRI in predicting disease risk in adults with pre-disease.

Adipose triglyceride lipase is a major hepatic lipase that regulates triacylglycerol turnover and fatty acid signaling and partitioning.

UNLABELLED: Despite advances in our understanding of the ways in which nutrient oversupply and triacylglycerol (TAG) anabolism contribute to hepatic steatosis, little is known about the lipases responsible for regulating hepatic TAG turnover. Recent studies have identified adipose triglyceride lipase (ATGL) as a major lipase in adipose tissue, although its role in the liver is largely unknown. Thus, we tested the contribution of ATGL to hepatic lipid metabolism and signaling. Adenovirus-mediated knockdown of hepatic ATGL resulted in steatosis in mice and decreased hydrolysis of TAG in primary hepatocyte cultures and in vitro assays. In addition to altering TAG hydrolysis, ATGL was shown to play a significant role in partitioning hydrolyzed fatty acids between metabolic pathways. Although ATGL gain and loss of function did not alter hepatic TAG secretion, fatty acid oxidation was increased by ATGL overexpression and decreased by ATGL knockdown. The effects on fatty acid oxidation coincided with decreased expression of peroxisome proliferator-activated receptor α (PPAR-α) and its target genes in mice with suppressed hepatic ATGL expression. However, PPAR-α agonism was unable to normalize the effects of ATGL knockdown on PPAR-α target gene expression, and this suggests that ATGL influences PPAR-α activity independently of ligand-induced activation. CONCLUSION: Taken together, these data show that ATGL is a major hepatic TAG lipase that plays an integral role in fatty acid partitioning and signaling to control energy metabolism.

Lipocalin 2 is a selective modulator of peroxisome proliferator-activated receptor-gamma activation and function in lipid homeostasis and energy expenditure.

We have previously identified lipocalin 2 (Lcn2) as a cytokine playing a critical role in the regulation of body fat mass, lipid metabolism, and insulin resistance. Lcn2 deficiency reduces PPARγ gene expression in adipocytes. In this study, we investigated the role of Lcn2 in PPARγ activation and function via assessing the insulin sensitization and fatty acid (FA) homeostasis of PPARγ agonist in high-fat diet (HFD)-induced obesity in Lcn2(-/-) mice. We found that rosiglitazone (Rosi) significantly improved insulin sensitivity in Lcn2(-/-) mice as effectively as in wild-type (WT) mice; unfed-state levels of blood glucose, free FAs, and triglycerides (TGs) were significantly reduced after a 25-d treatment of Rosi in Lcn2(-/-) mice. However, Rosi action on fat deposition and FA homeostasis was altered; Rosi-induced body weight and subcutaneous fat gain and liver lipid accumulation were markedly lessened in Lcn2(-/-) mice. The results of in vivo metabolic labeling showed that Rosi markedly reduced de novo lipogenesis in adipose tissue of Lcn2(-/-) mice. In brown adipose tissue (BAT), the expression of the genes functioning in TG hydrolysis and mitochondrial oxidation was up-regulated more in Lcn2(-/-) than in WT mice. Most strikingly, Rosi stimulated significantly higher levels of uncoupling protein-1 expression in BAT, and completely rescued cold intolerance in Lcn2(-/-) mice. We demonstrate that Lcn2 is a critical selective modulator of PPARγ activation and function in lipid homeostasis and energy expenditure.

Perspectives on the systematic review for the 2020 Dietary Reference Intakes for Koreans for calcium.

An accurate assessment of the recommended calcium (Ca) intake may contribute to reducing the risk of fractures and chronic diseases, ultimately improving quality of life. This review was performed to summarize key findings of Ca studies, investigate the effect of Ca intake on health outcomes, and determine the adequacy of evidence to revise the 2015 Dietary Reference Intakes for Koreans (KDRIs) for Ca in 2020. Databases were searched for intervention studies that assessed health outcomes by providing Ca in diets or as supplements. The framework of the systematic review comprised conducting literature searches, data extraction, quality assessment of the literature, and summarizing key findings relevant to set the Estimated Average Requirement (EAR) and Tolerable Upper Intake Level (UL) for Ca for the 2020 KDRI. The final search was performed in June 2019. A total of 13,309 studies were identified through databases and manual search. Sixtyfive studies were included in the final quality assessment and were summarized according to health indicators. As bone health was used as an indicator of the EAR for Ca, literature reports on bone health were further categorized by the life-cycle stage of the participants. This systematic review did not find new evidence that could be applied to the general Korean adult population, including postmenopausal women, for defining a new EAR for Ca in the 2020 KDRIs. Evidence in most of the reviewed literature was considered weak; however, some evidence was found that could improve the criteria on how the EAR for Ca was determined in children and adolescents. A review of the literature for the 2020 KDRIs for Ca did not find strong evidence in order to change the recommended values of the 2015 KDRIs. More clinical interventions are required among Koreans to strengthen the body of evidence to warrant the revision of the KDRIs.

Effect of the Timing of Nutritional Support Team Intervention on Nutritional Status on Patients Receiving Enteral Nutrition.

Many hospitalized patients usually have a high risk of malnutrition, which delays the therapy process and can lead to severe complications. Despite of the potential benefits, the effects of timely intervention by nutrition support team (NST) on the nutritional status of admitted patients are not well established. This study aimed to compare the nutritional status between patients with early and delayed NST supports and to assess the effect of the timing of NST support initiation on the nutritional status of enteral nutrition patients. In a simple comparison between the two groups, the early NST intervention group had shorter hospital stays and fewer tube feeding periods than the delayed NST intervention group. The increase in the amount of energy intake from first to last NST intervention was 182.3 kcal in patients in the early NST intervention group, higher than that in patients in the delayed intervention group (p = 0.042). The extent of reduction in serum albumin and hemoglobin levels between the initial and last NST intervention tended to be lower in the early NST intervention group than in the delayed NST intervention group. The mean odds ratio for the patients who were severely malnourished in the early NST intervention group was 0.142 (95% confidence interval, 0.045-0.450) after adjusting for hospital stay and age. The results of this study indicate that early NST intervention can improve patients' overall nutritional status.

Hepatic long-chain acyl-CoA synthetase 5 mediates fatty acid channeling between anabolic and catabolic pathways.

Long-chain acyl-CoA synthetases (ACSLs) and fatty acid transport proteins (FATPs) activate fatty acids (FAs) to acyl-CoAs prior to their downstream metabolism. Of numerous ACSL and FATP isoforms, ACSL5 is expressed predominantly in tissues with high rates of triacylglycerol (TAG) synthesis, suggesting it may have an anabolic role in lipid metabolism. To characterize the role of ACSL5 in hepatic energy metabolism, we used small interference RNA (siRNA) to knock down ACSL5 in rat primary hepatocytes. Compared with cells transfected with control siRNA, suppression of ACSL5 expression significantly decreased FA-induced lipid droplet formation. These findings were further extended with metabolic labeling studies showing that ACSL5 knockdown resulted in decreased [1-(14)C]oleic acid or acetic acid incorporation into intracellular TAG, phospholipids, and cholesterol esters without altering FA uptake or lipogenic gene expression. ACSL5 knockdown also decreased hepatic TAG secretion proportionate to the observed decrease in neutral lipid synthesis. ACSL5 knockdown did not alter lipid turnover or mediate the effects of insulin on lipid metabolism. Hepatocytes treated with ACSL5 siRNA had increased rates of FA oxidation without changing PPAR-α activity and target gene expression. These results suggest that ACSL5 activates and channels FAs toward anabolic pathways and, therefore, is an important branch point in hepatic FA metabolism.

Suppression of long chain acyl-CoA synthetase 3 decreases hepatic de novo fatty acid synthesis through decreased transcriptional activity.

Long chain acyl-CoA synthetases (ACSL) and fatty acid transport proteins (FATP) activate fatty acids to acyl-CoAs in the initial step of fatty acid metabolism. Numerous isoforms of ACSL and FATP exist with different tissue distribution patterns, intracellular locations, and substrate preferences, suggesting that each isoform has distinct functions in channeling fatty acids into different metabolic pathways. Because fatty acids, acyl-CoAs, and downstream lipid metabolites regulate various transcription factors that control hepatic energy metabolism, we hypothesized that ACSL or FATP isoforms differentially regulate hepatic gene expression. Using small interference RNA (siRNA), we knocked down each liver-specific ACSL and FATP isoform in rat primary hepatocyte cultures and subsequently analyzed reporter gene activity of numerous transcription factors and performed quantitative mRNA analysis of their target genes. Compared with control cells, which were transfected with control siRNA, knockdown of acyl-CoA synthetase 3 (ACSL3) significantly decreased reporter gene activity of several lipogenic transcription factors such as peroxisome proliferator activation receptor-gamma, carbohydrate-responsive element-binding protein, sterol regulatory element-binding protein-1c, and liver X receptor-alpha and the expression of their target genes. These findings were further supported by metabolic labeling studies that showed [1-(14)C]acetate incorporation into lipid extracts was decreased in cells treated with ACSL3 siRNAs and that ACSL3 expression is up-regulated in ob/ob mice and mice fed a high sucrose diet. ACSL3 knockdown decreased total acyl-CoA synthetase activity without substantially altering the expression of other ACSL isoforms. In summary, these results identify a novel role for ACSL3 in mediating transcriptional control of hepatic lipogenesis.

Suppression of long chain acyl-CoA synthetase blocks intracellular fatty acid flux and glucose uptake in skeletal myotubes.

Alterations in fatty acid metabolism are associated with impaired glucose uptake in skeletal muscle. Long-chain acyl-CoA synthetase (Acsl) 6 is the one of the Acsl isoforms expressed in skeletal muscle although its role in muscle energy metabolism has not been studied. Thus, the aims of this study were to investigate the role of Acsl6 in fatty acid partitioning and glucose uptake in differentiated skeletal myotubes using a siRNA-mediated knockdown approach. Compared with cells transfected with control siRNA, cells transfected with Acsl6 siRNA exhibited reduced intracellular triacylglycerol (TAG) accumulation. The initial rate of [1­14C]­oleic acid uptake was not altered while the incorporation of [1­14C]­acetic acids into total cellular lipids decreased under Acsl6 knockdown (p < 0.05). In a metabolic labeling study, Acsl6 suppression decreased the incorporation of [1­14C]­oleic acids and [1­14C]­acetic acids into TAG and diacylglycerol (DAG) (p < 0.05). During the chase period of a pulse-chase experiment, Acsl6 suppression increased the intracellular free fatty acids and decreased the fatty acid channeling toward the reacylation of TAG (p < 0.05). The incorporation of the labeled fatty acids into acid-soluble metabolites, ß-oxidation product, was not changed under Acsl6 knockdown. Acsl6 siRNA decreased the insulin-induced uptake of [1­14C]­2­deoxyglucose (p < 0.05) but did not change the glucose uptake in the presence of acipimox, inhibitor of lipolysis. Suppression of Acsl6 deteriorated Akt phosphorylation and Glut4 mRNA expression in response to insulin. These results suggest that Acsl6 activates and channels fatty acids toward anabolic pathways and has a role in glucose and fatty acid cycling through the re-esterification of fatty acids in skeletal muscle.

Associations of Dietary Intake with Cardiovascular Disease, Blood Pressure, and Lipid Profile in the Korean Population: a Systematic Review and Meta-Analysis.

OBJECTIVE: Previous studies have separately reported the contributions of dietary factors to the risk of cardiovascular disease (CVD) and its markers, including blood pressure (BP) and lipid profile. This study systematically reviewed the current evidence on this issue in the Korean population. METHODS: Sixty-two studies from PubMed and Embase were included in this meta-analysis. We performed a random-effects model to analyze pooled odds ratios (ORs) and hazard ratios (HRs) and their 95% confidence intervals (CIs) for the consumption of 14 food items, three macro- and eight micro-nutrients, two dietary patterns, and three dietary indices. RESULTS: An analysis of pooled effect sizes from at least four individual study populations showed significant associations between coffee consumption and CVD (OR/HR, 0.71; 95% CI, 0.52-0.97) and elevated/high triglycerides (TG) (OR, 0.84; 95% CI, 0.78-0.90), sugar-sweetened beverage intake and elevated BP (OR/HR, 1.20; 95% CI, 1.09-1.33), and milk and dairy intake and elevated/high TG and low high-density lipoprotein cholesterol (HDL-C) (OR/HR, 0.82; 95% CI, 0.76-0.89 for both). Carbohydrate consumption and the low-carbohydrate-diet score were consistently related to an approximately 25% risk reduction for elevated TG and low HDL-C. A lower risk of elevated total cholesterol, but not low-density lipoprotein, was additionally observed for those with a higher low-carbohydrate-diet score. A healthy dietary pattern was only associated with a reduced risk of elevated TG in the Korea National Cancer Screenee Cohort (OR, 0.81; 95% CI, 0.67-0.98). CONCLUSION: This study showed that milk and dairy and coffee had protective effects for CVD and its risk factors, such as BP and lipid profile, while sugar-sweetened beverages exerted harmful effects.

All-Cause Mortality and Cardiovascular Death between Statins and Omega-3 Supplementation: A Meta-Analysis and Network Meta-Analysis from 55 Randomized Controlled Trials.

Statins and omega-3 supplementation have shown potential benefits in preventing cardiovascular disease (CVD), but their comparative effects on mortality outcomes, in addition to primary and secondary prevention and mixed population, have not been investigated. This study aimed to examine the effect of statins and omega-3 supplementation and indirectly compare the effects of statin use and omega-3 fatty acids on all-cause mortality and CVD death. We included randomized controlled trials (RCTs) from meta-analyses published until December 2019. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated to indirectly compare the effect of statin use versus omega-3 supplementation in a frequentist network meta-analysis. In total, 55 RCTs were included in the final analysis. Compared with placebo, statins were significantly associated with a decreased the risk of all-cause mortality (RR = 0.90, 95% CI = 0.86-0.94) and CVD death (RR = 0.86, 95% CI = 0.80-0.92), while omega-3 supplementation showed a borderline effect on all-cause mortality (RR = 0.97, 95% CI = 0.94-1.01) but were significantly associated with a reduced risk of CVD death (RR = 0.92, 95% CI = 0.87-0.98) in the meta-analysis. The network meta-analysis found that all-cause mortality was significantly different between statin use and omega-3 supplementation for overall population (RR = 0.91, 95% CI = 0.85-0.98), but borderline for primary prevention and mixed population and nonsignificant for secondary prevention. Furthermore, there were borderline differences between statin use and omega-3 supplementation in CVD death in the total population (RR = 0.92, 95% CI = 0.82-1.04) and primary prevention (RR = 0.85, 95% CI = 0.68-1.05), but nonsignificant differences in secondary prevention (RR = 0.97, 95% CI = 0.66-1.43) and mixed population (RR = 0.92, 95% CI = 0.75-1.14). To summarize, statin use might be associated with a lower risk of all-cause mortality than omega-3 supplementation. Future direct comparisons between statin use and omega-3 supplementation are required to confirm the findings.

Dried plum polyphenols attenuate the detrimental effects of TNF-alpha on osteoblast function coincident with up-regulation of Runx2, Osterix and IGF-I.

Previous studies have demonstrated that dried plums which contain high amounts of polyphenols can restore bone mass and structure, and significantly increase indices of bone formation. The purpose of this study was to determine how dried plum polyphenols influence osteoblast activity and mineralized nodule formation under normal and inflammatory conditions. MC3T3-E1 cells were plated and pretreated with dried plum polyphenols (0, 2.5, 5, 10 and 20 microg/ml) and 24 h later stimulated with TNF-alpha (0 or 1.0 ng/ml). The 5, 10 and 20 microg/ml doses of polyphenols significantly increased intracellular ALP activity under normal conditions at 7 and 14 days, and restored the TNF-alpha-induced suppression of intracellular ALP activity by 14 days (P<.001). Polyphenols also increased mineralized nodule formation under normal and inflammatory conditions. In the absence of TNF-alpha, 5 microg/ml of polyphenols significantly up-regulated the growth factor, IGF-I, compared to controls, and the 5 and 10 microg/ml doses increased the expression of lysyl oxidase involved in collagen crosslinking. TNF-alpha decreased the expression of Runx2, Osterix and IGF-I, and polyphenols restored their mRNA levels to that of the controls. Although TNF-alpha failed to alter lysyl oxidase at 18 h, the polyphenols up-regulated its expression (P<.05) in the presence of TNF-alpha. As expected, TNF-alpha up-regulated RANKL mRNA and polyphenols suppressed RANKL expression without altering OPG. Based on these findings, we conclude that dried plum polyphenols enhance osteoblast activity and function by up-regulating Runx2, Osterix and IGF-I and increasing lysyl oxidase expression, and at the same time attenuate osteoclastogenesis signaling.

Genetically Mediated Lipid Metabolism and Risk of Insulin Resistance: Insights from Mendelian Randomization Studies.

Dysregulated lipid metabolism, characterized by higher levels of circulating triglycerides, higher levels of small, low density lipoprotein, and accumulation of intracellular lipids, is linked to insulin resistance and related complications such as type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVD). Considering that various metabolic, genetic, and environmental factors are involved in the development of T2DM and CVD, the causalities of these diseases are often confounded. In recent years, Mendelian randomization (MR) studies coupling genetic data in population studies have revealed new insights into the risk factors influencing the development of CVD and T2DM. This review briefly conceptualizes MR and summarizes the genetic traits related to lipid metabolism by evaluating their effects on the indicators of insulin resistance based on the results of recent MR studies. The data from the MR study cases referred to in this review indicate that the causal associations between lipid status and insulin resistance in MR studies are not conclusive. Furthermore, available data on Asian ethnicities, including Korean, are very limited. More genome-wide association studies and MR studies on Asian populations should be conducted to identify Asian- or Korean-specific lipid traits in the development of insulin resistance and T2DM. The present review discusses certain studies that investigated genetic variants related to nutrient intake that can modify lipid metabolism outcomes. Up-to-date inferences on the causal association between lipids and insulin resistance using MR should be interpreted with caution because of several limitations, including pleiotropic effects and lack of information on genotype and ethnicity.

Erratum: Total energy intake according to the level of skeletal muscle mass in Korean adults aged 30 years and older: an analysis of the Korean National Health and Nutrition Examination Surveys (KNHANES) 2008-2011.

[This corrects the article on p. 222 in vol. 12, PMID: 29854328.].

Erratum: A Vegetable and Fish Dietary Pattern Is Positively Associated with Skeletal Muscle Mass in Korean Men.

[This corrects the article on p. 1 in vol. 8, PMID: 30746343.].

A Vegetable and Fish Dietary Pattern Is Positively Associated with Skeletal Muscle Mass in Korean Men.

Isolating the effects of a single nutrient or food in relation to health outcomes including increased skeletal muscle mass is a challenging task because dietary constituents are highly correlated and synergistic. Hence, diet pattern analysis may be used to investigate the role of certain diets in health outcomes. The present study investigated the dietary patterns and their relationship to skeletal muscle mass in Korean adults. Data were extracted from the 2008-2011 Korea National Health and Nutrition Examination Surveys. To explore the dietary patterns of the study subjects, factor analysis was performed using data obtained from a 24-hour recall. The skeletal muscle index according to dietary pattern scores was then investigated to estimate the changes in skeletal muscle mass. Three patterns were initially identified from the factor analysis. Of these vegetables and fish (VF) pattern was the primary factor with high reliability and was a common factor in sex-separated analyses. The VF pattern scores were positively associated with increased skeletal muscle mass in both men and women. Further analysis according to quartile levels of VF pattern scores showed a positive association between skeletal muscle mass and VF pattern in men but not in women. These results suggest that dietary patterns focused on vegetables and seafoods may contribute to increased skeletal muscle mass in Korean men but that sex difference should be considered in nutrition care for skeletal muscle health.

Trans fats: foods, facts, and biology.

Trans fatty acids (TFAs) have made headlines because of the federal government's recent regulatory steps to reduce dietary intake of these potentially dangerous compounds. This review will focus on the chemistry of TFAs, their dietary sources, their association with various chronic diseases, and the possible mechanisms explaining their biological effects.