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Background Cardiac rehabilitation (CR) is recommended for patients with cardiovascular disease. However, the participation and completion rates for hospital-based CR are low, and home-based CR has been suggested as an alternative. This study aimed to develop a home-based CR program and assess its feasibility over a 6-week period in patients with left ventricular dysfunction or a history of myocardial infarction (MI).Methods The study consisted of two parts: Pilot Study 1 focused on developing an exercise protocol, while Study 2 aimed to assess the feasibility of a 6-week home-based CR program. Eight patients participated in Study 1 and 16 participated in Study 2. The home-based CR exercise program in Study 2 was developed based on the results of Study 1 and included two exercise education sessions and four telephone counseling sessions.Results Participants expressed overall satisfaction with the exercise program in Study 1. Heart rate increased in response to exercise, but this did not correspond with perceived exertion. In Study 2, 13 out of 16 participants (81.3%) completed the 6-week home-based CR program, with a participation rate of 100% in both exercise education and phone counseling sessions. Adherence to the exercise protocol was 83.1% and no serious adverse events were observed. At the beginning of the study, only three out of 13 participants (23.1%) met the requirements for both aerobic and resistance exercises, but at the end of the 6-week program, 10 out of 13 participants (76.9%) fulfilled the requirements.Conclusion The exercise program developed in this study was safe and feasible, and the 6-week home-based CR program was feasible and effective in increasing the physical activity levels of patients with left ventricular dysfunction without any reported adverse effects.

Non-alcoholic fatty liver disease (NAFLD) is frequently associated with obesity, insulin resistance, and endoplasmic reticulum (ER) stress. Elevated circulating levels of the hepatokine leukocyte cell-derived chemotaxin-2 (LECT2) have also been noted in NAFLD; however, the mechanism underlying this association is unclear. To investigate a possible link between ER stress/unfolded protein response (UPR) signaling and LECT2 secretion, HepG2 cells were incubated with ER stress inducers with or without an ER stress-reducing chemical chaperone. Additionally, UPR pathway genes were knocked down and overexpressed, and a ChIP assay was performed. In diet-induced obese mice, hepatic expression of LECT2 and activating transcription factor 4 (ATF4) was measured. In HepG2 cells, LECT2 expression was increased by ER stressors, an effect blocked by the chemical chaperone. Among UPR pathway proteins, only knockdown of ATF4 suppressed ER stress-induced LECT2 expression, while overexpression of ATF4 enhanced LECT2 expression. The ChIP assay revealed that ATF4 binds to three putative binding sites on the LECT2 promoter and binding is promoted by an ER stress inducer. In steatotic livers of obese mice, LECT2 and ATF4 expression was concomitantly elevated. Our data indicate that activation of ER stress/UPR signaling induces LECT2 expression in steatotic liver; specifically, ATF4 appears to mediate upregulation of LECT2 transcription.

Activated dendritic cells (DCs) undergo significant metabolic reprogramming, which is characterized by an increase in aerobic glycolysis and a concurrent progressive loss of oxidative phosphorylation. The modulation of metabolic reprogramming is believed to be closely related to the function of DCs. Vitamin D has been reported to inhibit the maturation of DCs. DC dysfunction has been reported in diabetic patients, and hyperglycemia is associated with impaired glycolytic metabolism in immune cells. Therefore, vitamin D and diabetes may affect intracellular metabolism, thereby regulating the activity of DCs. We investigated the effect of in vitro treatment of 1,25-dihydroxyvitamin D

Vitamin D affects differentiation, maturation, and activation of dendritic cells (DCs). Obesity-related immune dysfunction is associated with metabolic changes in immune cells. Objectives of the study are to investigate the effects of vitamin D and obesity on immune responses and markers related to immunometabolism of bone marrow-derived dendritic cells (BMDCs). Bone marrow cells (BMCs) were isolated from lean and obese mice, and BMDCs were generated by culturing BMCs with rmGM-CSF. BMDCs were treated with 1 or 10 nM of 1,25-dihydroxyvitamin D

OBJECTIVES: DTC genetic test results are provided directly to consumers without involvement of medical institution, which allows individual access to genetic information. Although studies have been conducted to determine the effects of genetic background recognition on behavioral changes, the effectiveness of DTC test on dietary change remains unclear. In this study, we examined the impact of disclosing DTC results on dietary intake using the Healthy Eating Index (HEI) as an indicator of diet quality. METHODS: A total of 100 disease-free healthy adults (50 male and 50 female) aged 25–35 y were stratified by sex, BMI (body mass index, kg/m(2)) and genetic risk, then randomly assigned into two groups. The intervention group (n = 65) was informed of the DTC test results on body fat mass (FTO, MC4R, BDNF), while the control group (n = 35, CON) was not. Based on the genetic risks reported, the intervention group was classified into Intervention-Non Risk (low risk, INR) or Intervention-Risk (borderline and high risk, IR) groups. Anthropometric and dietary intake data were collected at baseline, 1, 2, 3, and 6 mo-time point. Diet quality was evaluated by the HEI 2015, which is consisted of 13 dietary components that reflects the key recommendations by the 2015–2020 Dietary Guidelines for Americans. RESULTS: Participants with genetic risks (IR) regarding the MC4R gene showed a significant decrease in body weight (kg) and BMI compared to the INR at 1 and 2 mo. In addition, WHR ratio (%) was decreased significantly in the IR compared to the INR at 3 mo. Regarding diet quality, the HEI of the IR was higher than that of the INR at 3 mo in female subjects (57.2 ± 5.36 vs. 51.3 ± 4.8). Among female subjects, dietary fat intake tended to increase in the INR compared to the CON (5.91 ± 14.46 vs. -1.93 ± 8.88). Saturated fatty acids intake increased significantly in the INR compared to IR at 3 mo time point. CONCLUSIONS: In conclusion, following the recognition of DTC results, female subjects with genetic risk for high BMI showed a decrease in body weight and WHR ratio compared to those with low genetic risk. The decrease in weight and WHR ratio might be attributed to healthier dietary intake in the risk group. FUNDING SOURCES: Supported by Seoul National University Research Grant in 2018 (350–20,180,049).

Inflammatory bowel disease (IBD) often accompanies vitamin D deficiency, and vitamin D supplementation ameliorates IBD symptoms in animal models and humans. Because altered vitamin D metabolism has been reported in obesity, we hypothesized that the effects of vitamin D on the development of IBD would be different between obese and control mice. Five-week-old male C57BL/6N mice were divided into 4 groups and fed a diet differing in fat content (10% or 45%, normal diet [ND] or high-fat diet [HFD]) and vitamin D content (1000 or 10 000 IU/kg of diet, vDC or vDS) for 14 weeks. At week 13, colitis was induced by administration of 2% dextran sodium sulfate for 7 days. Histology score tended to be lower in the HFD-vDS group than HFD-vDC group, but there was no effect of vitamin D on the ND group. Colonic Cldn1 and Cyp27b1 mRNA levels were higher in the HFD-vDS than HFD-vDC group, but these effects of vitamin D were not observed in the ND group. The serum 25-hydroxy vitamin D levels were negatively correlated with the histology score in the HFD group but not in the ND group. Overall, these results suggest that vitamin D supplementation partially prevents the histological damage of the colon in obese mice but not in control mice. This effect might be mediated by increased colonic Cyp27b1 levels, leading to upregulation of local 1,25-dihydroxy vitamin D production.

Results from microarray analyzes have shown that both vitamin E deficiency and supplementation have a significant impact on the gene expression of various tissues and cells. Genes that were modulated by vitamin E supplementation were different depending on the tissue, which suggested that changes in gene expression are reflective of tissue function and the tissue-specific regulation of vitamin E. In addition, the magnitude of gene expression and types of genes whose expression was altered were differentially affected by the vitamin E forms used for intervention. Metabolite analyzes have provided better understanding of the vitamin E metabolic pathway and have established evidence for the regulation of energy, lipid, and glucose metabolism by vitamin E. However, there are a limited number of studies that have applied advanced genomics, proteomics, and metabolomics technologies to investigate vitamin E's biological functions and mechanisms of action. In this review, the effects of vitamin E on gene and protein expression investigated by microarray, transcriptome, and proteomics analysis are discussed. © 2019 IUBMB Life, 71(4):442-455, 2019.

BACKGROUND/OBJECTIVES Obesity is associated with the impaired regulation of T cells characterized by increased numbers of Th1 and Th17 cells and the dysregulation of vitamin D metabolism. Both obesity and vitamin D have been reported to affect autophagy; however, a limited number of studies have investigated the effects of vitamin D on T cell autophagy in obese mice. Therefore, we aimed to determine whether in vitro treatment with vitamin D affects the proliferation, function, and autophagy of T cells from obese and control mice. MATERIALS/METHODS Five-week-old male C57BL/6 mice were fed control or high-fat diets (10% or 45% kcal fat: CON or HFDs, respectively) for 12 weeks. Purified T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either 10 nM 1,25(OH)2D3 or 0.1% ethanol (vehicle control). The proliferative response; expression of CD25, Foxp3, RORγt, and autophagy-related proteins (LC3A/B, SQSTM1/P62, BECLIN-1, ATG12); and the production of interferon (IFN)-γ, interleukin (IL)-4, IL-17A, and IL-10 by T cells were measured. RESULTS Compared with the CON group, T cell proliferation tended to be lower, and the production of IFN-γ was higher in the HFD group. IL-17A production was reduced by 1,25(OH)2D3 treatment in both groups. The LC3 II/I ratio was higher in the HFD group than the CON group, but P62 did not differ. We observed no effect of vitamin D treatment on T cell autophagy. CONCLUSIONS Our findings suggest that diet-induced obesity may impair the function and inhibit autophagy of T cells, possibly leading to the dysregulation of T cell homeostasis, which may be behind the aggravation of inflammation commonly observed in obesity.

Obesity is associated with the dysregulation of vitamin D metabolism and altered immune responses in bone marrow-derived dendritic cells (BMDCs). Vitamin D can affect the differentiation, maturation, and activation of dendritic cells (DCs) and regulate autophagy via vitamin D receptor signaling. Autophagy was shown to be involved in the functions of DCs. We investigated the effects of dietary vitamin D supplementation and in vitro 1,25-dihydroxyvitamin D

Obesity is associated with an impaired balance of CD4+ T cell subsets. Both vitamin D and obesity have been reported to affect the mTOR pathway. In this study, we investigated the effects of vitamin D on CD4+ T cell subsets and the mTOR pathway. Ten-week-old male C57BL/6 mice were divided into four groups and fed diets with different fat (control or high-fat diets: CON or HFD) and vitamin D contents (vitamin D control or supplemented diets: vDC or vDS) for 12 weeks. T cells purified by negative selection were stimulated with anti-CD3/anti-CD28 mAbs and cultured for 48 h. The percentage of CD4+IL-17+ T cells was higher in the vDS than vDC groups. The CD4+CD25+Foxp3+ T cells percentage was higher in HFD than CON groups. The phospho-p70S6K/total-p70S6K ratio was lower in vDS than vDC, but the phospho-AKT/total-AKT ratio was higher in vDS than vDC groups. Hif1α mRNA levels were lower in vDS than vDC groups. These findings suggest HIF1α plays an important role in vitamin-D-mediated regulation of glucose metabolism in T cells, and dietary vitamin D supplementation may contribute to the maintenance of immune homeostasis by regulating the mTOR pathway in T cells.

Obesity is associated with the dysregulation of vitamin D metabolism and altered immune responses in bone marrow-derived dendritic cells (BMDCs). Vitamin D can affect the differentiation, maturation, and activation of dendritic cells (DCs) and regulate autophagy via vitamin D receptor signaling. Autophagy was shown to be involved in the functions of DCs. We investigated the effects of dietary vitamin D supplementation and in vitro 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) treatment on autophagy in BMDCs from control diet (CON)-fed lean and high-fat diet (HFD)-induced obese mice. C57BL/6 male mice were fed CON or HFD with 10% or 45% kcal fat, respectively, supplemented with 1,000 or 10,000 IU vitamin D/kg diet (vDC or vDS) for 12 weeks. BMDCs were generated by culturing bone marrow cells from the mice with 20 ng/mL rmGM-CSF and treated with 1 nM 1,25(OH)2D3. Maturation of BMDCs was induced by lipopolysaccharide (50 ng/mL) stimulation. Treatment with 1,25(OH)2D3 inhibited the expression of phenotypes related to DC function (MHC class Ⅱ, CD86, CD80) and production of IL-12p70 by BMDCs from control and obese mice, regardless of dietary vitamin D supplementation. LC3Ⅱ/Ⅰ and VPS34 protein levels increased, and p62 expression decreased, after 1,25(OH)2D3 treatment of the BMDCs in CON-vDC only. Vdr mRNA levels decreased following 1,25(OH)2D3 treatment of BMDCs in the HFD-vDC. In conclusion, autophagy flux was increased by 1,25(OH)2D3 treatment of the BMDCs in CON-vDC but not in the HFD-vDC group. This suggests that the decreased expression of Vdr following 1,25(OH)2D3 treatment might have affected autophagy flux in BMDCs from obese mice.

Adipose tissue is composed of diverse cell types and plays a major role in energy homeostasis and inflammation at the local and systemic levels. Adipose tissue serves as the main site for vitamin D storage and is among the most important extraskeletal targets of vitamin D which can modulate multiple aspects of adipose tissue biology. Vitamin D may exert inhibitory or stimulatory effects on adipocyte differentiation depending on cell type, stage of differentiation, and the treatment time point. Moreover, vitamin D controls energy metabolism in adipose tissue by affecting fatty acid oxidation, expression of uncoupling proteins, insulin resistance, and adipokine production. Adipose tissue inflammation can have a significant impact on the metabolic disorders often associated with obesity, and vitamin D can modulate the inflammatory response of immune cells and adipocytes within the adipose tissue. This review discusses the role of adipose tissue in vitamin D metabolism, as well as the regulatory role of vitamin D in adipocyte differentiation, adipose tissue energy metabolism, and inflammation, thereby providing insights into the importance of vitamin D in adipose tissue biology.

BackgroundFor chronic kidney disease (CKD) patients, management of nutritional status is critical for delaying progression to end-stage renal disease. The purpose of this study is to provide the basis for personalized nutritional intervention in pre-dialysis patients by comparing the foods contributing to nutrients intake, nutritional status and potential dietary inflammation of CKD patients according to the diabetes mellitus (DM) comorbidity and CKD stage.MethodsTwo hundred fifty-six outpatients referred to the Department of Nephrology at SNUH from Feb 2016 to Jan 2017 were included. Subjects on dialysis and those who had undergone kidney transplantation were excluded. Bioelectrical impedance analysis (BIA), subjective global assessment (SGA), dietary intake, and biochemical parameters were collected. Subjects were classified into 4 groups according to DM comorbidity (DM or Non-DM) and CKD stage (Early or Late) by kidney function. Two-way analysis of variance and multinomial logistic regression analysis were performed for statistical analysis.ResultsTotal number of malnourished patients was 31 (12.1%), and all of them were moderately malnourished according to SGA. The body mass index (BMI) of the DM-CKD group was significantly higher than the Non-DM-CKD group. The contribution of whole grains and legumes to protein intake in the DM-CKD group was greater than that in the Non-DM-CKD group. The DM- Early-CKD group consumed more whole grains and legumes compared with the Non-DM-Early-CKD group. The subjects in the lowest tertile for protein intake had lower phase angle, SGA score and serum albumin levels than those in the highest tertile. The potential for diet-induced inflammation did not differ among the groups.ConclusionsSignificant differences in intakes of whole grains and legumes between CKD patients with or without DM were observed. Since contribution of whole grains and legumes to phosphorus and potassium intake were significant, advice regarding whole grains and legumes may be needed in DM-CKD patients if phosphorus and potassium intake levels should be controlled. The nutritional status determined by BIA, SGA and serum albumin was found to be different depending on the protein intake. Understanding the characteristics of food sources can provide a basis for individualized nutritional intervention for CKD patients depending on the presence of diabetes.

Background Vitamin D deficiency has been often observed in obese persons. One of the mechanisms suggested for low vitamin D status in obesity was decreased bioavailability of vitamin D (VD) due to sequestration in adipose tissue. However, only few studies have investigated this mechanism via quantifying vitamin D levels from tissues from the obese. Methods Six-wk-old C57BL/6 mice were fed 10 or 45% kcal fat (CON or HFD) diets containing 50, 1000 or 25,000 IU vitamin D/kg diet (LVd, CVd or HVd) for 13 wks. Serum 25-hydroxyvitamin D (25(OH)D) levels were determined by radioimmunoassay and liver and adipose tissue cholecalciferol (VD) and 25-hydrocholecalciferol (25(OH)D) levels were measured by LC-MS/MS. mRNA levels of jejunal Mttp, Cd36, Sr-b1, Npc1l1, and Abca1 and liver and adipose tissue 25-hydroxylases (Cyp2r1 and Cyp27a1) were determined by real-time PCR. Results Serum 25(OH)D levels were affected by dietary vitamin D content but differential effects were observed between HFD and CON groups. When vitamin D intake was at a supplementary level, the HFD-HVd group had lower serum 25(OH)D levels than the CON-HVd group, while there was no significant difference between the HFD and CON groups fed LVd or CVd. Total amount of VD in liver and adipose tissue were significantly higher in HFD-HVd group compared with the CON-HVd group. However, no difference in total amount of tissue VD was observed between the CON and HFD groups fed CVd. In jejunum, mRNA levels of Mttp and Abca1 were significantly higher in HFD groups than CON groups. There was no difference in mRNA levels of liver 25-hydroxylases by both dietary fat amount and vitamin D content. Conclusion A significant amount of VD seemed to be stored in the liver and adipose tissue when dietary vitamin D is at a supplementation level; thus excess body adiposity could contribute to relatively low serum 25(OH)D level when vitamin D was supplemented.

OBJECTIVES: Genetic variation contributes to individual differences in food preference, dietary habit, and nutrient intake, thus affecting nutritional status. Although studies which showed the relevance between genetic differences and the intake of nutrients such as carotenoid, vitamin E, and fat are available, more studies are needed for implementation of precision nutrition. Objective of the study was to investigate genetic variations that are associated with nutrient intake and taste sensitivity. METHODS: A total of 100 healthy adults (50 men and 50 women) aged 25–35 y who were free of diseases were recruited. Anthropometric measurements, clinical parameters including CBC, lipid profile, glucose level, and liver function tests, dietary intake data using 3-day food record, and taste sensitivity for salty and sweet tastes were determined. A total of 800,000 single nucleotide polymorphisms (SNPs) were analyzed by Theragen Etex using Theragen Precision Medicine Research Array (PMRA) chips. RESULTS: A total of 577,164 qualified SNPs were analyzed and three SNPs that might have significant relevance with energy intake (rs75052357, rs1125186, rs73471118) were identified. Carriers of the C allele in rs75052357 (C > T), which is identified in IQGAP1 loci, showed significantly higher fat mass (CC: 16.16 ± 3.52 kg, TC: 14.26 ± 3.58 kg, TT: 12.43 ± 3.83 kg) and higher % body fat (CC: 25.68 ± 5.40%, TC: 22.79 ± 6.10%, TT: 20.60 ± 7.52%) despite a lower energy intake (CC: 1782.2 ± 445.5 kcal, TC: 2212.5 ± 424.1 kcal, TT: 2315.0 ± 892.6 kcal). Carriers of G allele in rs1125186 (G > C) had significantly higher fat mass (CC: 13.34 ± 16.22 kg, CG: 16.22 ± 3.48 kg, GG: 15.67 ± 3.63 kg) in spite of lower energy intake compared with CC carriers (CC: 2222.5 ± 515.9 kcal, CG: 1927.9 ± 452.6 kcal, GG: 1745.7 ± 476.7 kcal). Carriers of T allele in rs73471118 (C > T) had significantly higher energy intake (CC: 1815.5 ± 445.0 kcal, TC: 2726.5 ± 490.6 kcal), while having lower threshold for sweet taste (CC: 8.94 ± 8.51 g/L TC: 0.40 ± 0.00 g/L). CONCLUSIONS: Novel SNPs showing associations between energy consumption and fat mass or sugar taste sensitivity have been identified. This finding can help developing personalized recommendation for energy intake, however, further studies to delineate the mechanisms are needed. FUNDING SOURCES: Supported by Seoul National University Research Grant in 2018.

Background Dietary intervention at the early stage of chronic kidney disease (CKD) is important for preventing progression to the end-stage renal disease (ESRD). However, few studies have investigated dietary intake of CKD patients in non-dialysis stage. Therefore, we investigated the dietary intake of Korean non-dialysis CKD patients and aimed to establish baseline data for the development of dietary education and intervention strategies for CKD patients. Methods Three hundred fifty CKD patients who visited Seoul National University Hospital outpatient clinic from February 2016 to January 2017 were recruited for this cross-sectional study. Subjects on dialysis and those who had undergone kidney transplantation were excluded. Dietary intake, demographic information, and biochemical characteristics of 256 subjects who completed three-day dietary records were analyzed. Subjects were divided into four groups based on diabetes mellitus (DM) (DM-CKD and Non-DM-CKD groups) and kidney function (Early-CKD and Late-CKD groups). Results Total energy intake was lower in the Late-CKD group compared with the Early-CKD group. In men, carbohydrate intake was higher and protein and fat intakes tended to be lower in the Late-CKD group compared with the Early-CKD group. In women, carbohydrate intake tended to be lower in the DM-CKD group than the Non-DM-CKD group. Protein intake tended to be higher in the DM-CKD groups. Phosphorus and sodium intakes were higher in the DM-CKD groups compared with the Non-DM-CKD groups in women, and tended to be higher in the DM-CKD groups in men. Conclusion DM and kidney function affected energy and nutrient intakes. Subjects in the Late-CKD group consumed less energy than those in the Early-CKD group. Non-DM subjects seemed to restrict protein intake starting from the Early-CKD stage than subjects with DM. Subjects in this study had low energy and high sodium intakes compared with recommended levels. Protein intake was lower in advanced CKD patients, but their intake level was still higher than the recommendation. Dietary intervention strategies for non-dialysis CKD patients need to be customized depending on the presence of DM and kidney function., Graphical Abstract

Vitamin D has been reported to regulate the maturation and function of dendritic cells (DCs). Obesity was shown to be associated with the dysregulation of vitamin D metabolism and malfunction of DCs. We investigated the effects of in vitro 1,25(OH)

Summary Autoimmune diseases are a host of diseases characterized by abnormal immune response against normal tissues of the body. There are about 100 autoimmune diseases, and they are estimated to affect at least 3%–5% of population. While the etiology is still unclear, both genetic and environmental factors are recognized to play key roles in the disease development. Pharmaceutical therapies have substantially improved the disease control and prognosis. However, the adverse effects and high cost of the drugs limit their use. There has been an increasing interest in alternative and complementary means to improve the outcomes of conventional therapies in many autoimmune diseases. Diet as a modifiable factor has the potential to improve clinical outcomes for several major autoimmune diseases. This chapter provides a summary and analysis of both observational and experimental studies as well as perspectives on the role of nutrition in prevention and treatment of some of the most prominent autoimmune diseases.

Korean pine nut oil (PNO) has been reported to suppress appetite by increasing satiety hormone release. However, previous studies have rendered inconsistent results and there is lack of information on whether dietary Korean PNO affects the expression of satiety hormone receptors and hypothalamic neuropeptides. Therefore, our study sought to evaluate the chronic effects of Korean PNO on the long-term regulation of energy balance.Five-week-old male C57BL/6 mice were fed with control diets containing 10% kcal fat from Korean PNO or soybean oil (SBO) (PC or SC) or high-fat diets (HFDs) containing 35% kcal fat from lard and 10% kcal fat from Korean PNO or SBO (PHFD or SHFD) for 12 weeks. The expression of gastrointestinal satiety hormone receptors, hypothalamic neuropeptides, and genes related to intestinal lipid absorption and adipose lipid metabolism was then measured.There was no difference in the daily food intake between PNO- and SBO-fed mice; however, the PC and PHFD groups accumulated 30% and 18% less fat compared to SC and SHFD, respectively. Korean PNO-fed mice exhibited higher messenger RNA (mRNA) expression ofIn summary, Korean PNO attenuated body fat accumulation, and appeared to prevent HFD-induced dysregulation of the hypothalamic appetite-suppressing pathway.

Vitamin D status has been implicated in obesity and adipose tissue inflammation. In the present study, we explored the effects of dietary vitamin D supplementation on adipose tissue inflammation and immune cell population, and the effects of in vitro 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) treatment on pro-inflammatory cytokine production by stromal vascular cells (SVCs) and adipocytes in lean and high-fat diet-induced obese mice. The results show that epididymal fat Mcp-1 and Rantes mRNA levels, which were higher in obese mice compared with lean mice, were significantly down-regulated by vitamin D supplementation. While obese mice had higher numbers of macrophages and natural killer (NK) cells within adipose tissue, these remained unaltered by vitamin D supplementation. In accordance with these in vivo findings, the in vitro 1,25(OH)2D3 treatment decreased IL-6, MCP-1, and IL-1&beta, production by SVCs from obese mice, but not by adipocytes. In addition, 1,25(OH)2D3 treatment significantly decreased Tlr2 expression and increased mRNA levels of I&kappa, ba and Dusp1 in SVCs. These findings suggest that vitamin D supplementation attenuates inflammatory response in adipose tissue, especially in SVCs, possibly through inhibiting NF-&kappa, B and MAPK signaling pathways in SVCs but not by the inhibition of macrophage infiltration.

We investigated the anti-arthritic effects of the radiation mutant Perilla frutescens var. crispa leaf extract (SFE-M) and wild type leaf extract (SFE-W), both prepared by supercritical carbon dioxide (SC-CO2) extraction, on collagen antibody-induced arthritis (CAIA) in Balb/c mice. Animals were randomly divided into four groups: control, CAIA, CAIA + SFE-M (100 mg/kg/day), and CAIA + SFE-W (100 mg/kg/day). The mice were subjected to the respective treatments via oral gavage once daily for 4 days. Mice treated with SFE-M developed less severe arthritis than the CAIA mice. They showed significantly improved arthritic score, paw volume, and paw thickness compared to the CAIA mice from days 3 through 7. Furthermore, histopathological analysis of ankle for inflammation showed that SFE-M treatment reduced inflammatory cell infiltration and edema formation. Similarly, the neutrophil-to-lymphocyte ratio (NLR) in the whole blood was 37% lower in mice treated with SFE-M compared with the CAIA mice. However, treatment with SFE-W did not result in any significant difference compared with the CAIA group. In conclusion, SFE-M treatment delays the onset of arthritis and alleviates its clinical manifestations in CAIA mice.

We investigated the anti-arthritic effects of the radiation mutant Perilla frutescens var. crispa leaf extract (SFE-M) and wild type leaf extract (SFE-W), both prepared by supercritical carbon dioxide (SC-CO2) extraction, on collagen antibody-induced arthritis (CAIA) in Balb/c mice. Animals were randomly divided into four groups: control, CAIA, CAIA + SFE-M (100 mg/kg/day), and CAIA + SFE-W (100 mg/kg/day). The mice were subjected to the respective treatments via oral gavage once daily for 4 days. Mice treated with SFE-M developed less severe arthritis than the CAIA mice. They showed significantly improved arthritic score, paw volume, and paw thickness compared to the CAIA mice from days 3 through 7. Furthermore, histopathological analysis of ankle for inflammation showed that SFE-M treatment reduced inflammatory cell infiltration and edema formation. Similarly, the neutrophil-to-lymphocyte ratio (NLR) in the whole blood was 37% lower in mice treated with SFE-M compared with the CAIA mice. However, treatment with SFE-W did not result in any significant difference compared with the CAIA group. In conclusion, SFE-M treatment delays the onset of arthritis and alleviates its clinical manifestations in CAIA mice.

Vitamin D has an immunoregulatory effect on both innate and adaptive immunity. Contradictory results regarding vitamin D and natural killer (NK) cell functions have been reported with in vitro studies, but little is known about this in vivo. We investigated whether vitamin D levels (50, 1000 or 10,000 IU/kg of diet: DD, DC or DS) affect NK cell functions in mice fed a control or high-fat diet (10% or 45% kcal fat: CD or HFD) for 12 weeks. The splenic NK cell activity was significantly higher in the CD-DS group than the HFD-DS group, and the CD-DS group showed significantly higher NK cell activity compared with the CD-DD and CD-DC groups. However, no difference in NK cell activity was observed among the HFD groups fed different levels of vitamin D. The splenic population of NK cells was significantly higher in the CD-DS group than the HFD-DS group. There was no difference in the intracellular expression of IFN-γ and the surface expression of NKG2D and CD107a in NK cells by both dietary fat and vitamin D content. The splenic mRNA expression of Ifng and Ccl5 was significantly lower in the HFD groups compared with the CD groups, but there was no difference in the mRNA levels of Vdup1 and Vdr among the groups. Taken together, these results suggest that dietary vitamin D supplementation can modulate innate immunity by increasing NK activity in control mice but not in obese mice. This effect might be mediated through alternation of the splenic NK cell population.

Altered regulation of vitamin D metabolites, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D (1,25[OH]2D), was observed in high-fat diet (HFD)-induced obesity. We hypothesized that these HFD-induced changes in vitamin D metabolism would be reversed by decreasing fat mass through dietary intervention. Four-week-old C57BL/6J mice were assigned to 1 of 3 experimental diet groups: (1) the LL group was fed a control diet for 31 weeks, (2) the HH group was fed an HFD for 31 weeks, and (3) the HL group was fed HFD for 15 weeks then switched to the control diet for the remaining 16 weeks. The fat mass of the HL group decreased by 15% from the 14th to the 30th week. Serum 1,25(OH)2D level was significantly higher in the HH group than the LL group, whereas that of the HL group was intermediate to the 2 groups. Serum parathyroid hormone and renal 1-hydroxylase (Cyp27b1) mRNA levels, which are known to stimulate renal 1,25(OH)2D production, were significantly higher in the HH group than the LL group. After losing fat mass, the HL group had significantly lower renal Cyp27b1 mRNA levels than the HH group. No differences were found in serum 25-hydroxyvitamin D levels and mRNA levels of hepatic 25-hydroxylases. In adipose tissue, mRNA levels of 25-hydroxylase and vitamin D receptor were elevated in parallel to the adiposity. In conclusion, serum 1,25(OH)2D levels were closely associated with body adiposity, and reducing fat mass by changing to a lower-fat diet can reverse this obesity-associated increase in circulating 1,25(OH)2D levels.

Background: Serum vitamin B12 levels have been proposed as one of the survival prediction factors, although no survival analysis in metastatic cancer patients has been conducted yet. This s...

Calorie restriction (CR) has been reported to improve lipid metabolism and to decrease inflammatory diseases. However, most existing CR models use 30–50% calorie reduction, which is hard to achieve in humans. We investigated the effects of mild CR on lipid metabolism and inflammatory responses. Male C57BL/6 mice were fed control diet (10% kcal fat, Control) or high fat diet (60% kcal fat, HFD) ad libitum or reduced amount of control diet to achieve 15% CR for 16 wks. Body weights, white adipose tissue weights, liver triacylglycerol levels, and serum fetuin-A levels were lower in CR than in the Control. Serum adiponectin levels were higher in CR and lower in HFD compared with the Control. Liver and adipose tissue Mcp-1 mRNA levels were significantly lower in CR compared with the Control. Adipose tissue mRNA levels of Mcp-1, Il-6, Tnf-α and Socs3 were significantly higher in HFD than in the Control and CR, and levels of these negatively correlated with serum adiponectin levels. CR group had the lowest leptin levels and the highest liver Lepr expression, and Lepr mRNA levels positively correlated with liver Socs3 mRNA levels. Our findings showed that mild CR lowered adiposity which resulted in higher adiponectin and lower fetuin-A levels, and might have contributed to alleviation of inflammatory status in the liver and adipose tissue. Furthermore, mild CR might have affected leptin sensitivity by up-regulating Lepr expression.

Liver is the central organ for lipid metabolism. Anabolic pathways of triacylglycerol and cholesterol synthesis and catabolic pathway of fatty acid (FA) oxidation are regulated by the energy status of the body and nutrient and hormone levels. Adequate uptake of circulating free FAs and lipoproteins and efflux of lipoproteins by the liver are important for maintaining lipid balance. Several dietary extracts reportedly modulate the lipid metabolism in the liver by affecting the expression of enzymes and transcription factors involved in lipid metabolism. In this chapter, regulatory effects of resveratrol, berry extract polyphenol, green tea extract and epigallocatechin gallate, curcumin, and quercetin on lipid metabolism in the liver have been reviewed.

Vitamin E is a fat-soluble antioxidant that can protect the polyunsaturated fatty acids (PUFAs) in the membrane from oxidation, regulate the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), and modulate signal transduction. Immunomodulatory effects of vitamin E have been observed in animal and human models under normal and disease conditions. With advances in understating of the development, function, and regulation of dendritic cells (DCs), macrophages, natural killer (NK) cells, T cells, and B cells, recent studies have focused on vitamin E’s effects on specific immune cells. This review will summarize the immunological changes observed with vitamin E intervention in animals and humans, and then describe the cell-specific effects of vitamin E in order to understand the mechanisms of immunomodulation and implications of vitamin E for immunological diseases.

Direct-to-consumer genetic testing (DTC-GT) provides a means for consumers to gain insights into their genetic background and how it relates to their health without the involvement of medical institutions. In Korea, DTC-GT was introduced in 2016 in accordance with the legislation on Paragraph (3) 2 of Article 50 of the Bioethics and Safety Act. Only 12 genetic test items involving 46 genes were approved at first, but the approved items were expanded to 70 in November 2020. However, the genetic test items of DTC-GT services in Korea are still restricted to the wellness area, and access to disease risk related information is only permitted to medical institutions. Further, studies revealing the relationship between genotype differences and responses to nutrients, food components, or nutritional status are increasing, and this association appears to be robust for some genes. This strong association between genetic variations and nutrition suggests that DTC-GT can be used as an important tool by clinical nutritionists to gain insights into an individual's genetic susceptibilities and provide guidance on nutritional counseling and meal planning based on the patient's genetic information. This review summarized the history and current status of DTC-GT and investigated the relationship between genetic variations with associated phenotypic traits to clarify further the importance of DTC-GT in the field of clinical nutrition.