Water-Soluble Extract of Pacific Krill Prevents Triglyceride Accumulation in Adipocytes by Suppressing PPARγ and C/EBPα Expression

BACKGROUND: Pacific Krill (Euphausia pacifica) are small, red crustaceans, similar to shrimp, that flourish in the North Pacific and are eaten in Japan. METHODS AND FINDINGS: We investigated the effect of a water-soluble extract of Pacific Krill on adipocytes and discovered that this extract suppressed triglyceride accumulation in adipocytes. Furthermore, the water-soluble extract of Pacific Krill suppressed the expression of two master regulators of adipocyte differentiation, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT enhancer binding protein alpha (C/EBPα). C/EBPβ promotes PPARγ and C/EBPα expression, but the water-soluble extract of Pacific Krill did not inhibit the expression of C/EBPβ or C/EBPβ-mediated transcriptional activation. The Pacific Krill extract was more effective than a PPARγ antagonist in suppressing PPARγ and C/EBPα expression. CONCLUSIONS: These results indicated that the water-soluble extract of Pacific Krill was not simply a PPARγ antagonist, but that it prevented triglyceride accumulation in adipocytes by suppression of PPARγ and C/EBPα via a pathway that is independent of C/EBPβ

Dermoscopy for Tick Bite: Reconfirmation of the Usefulness for the Initial Diagnosis

Ticks transmit a variety of infectious diseases. Diagnosis requires verification of a tick's presence. Here, we describe a 61-year-old woman bitten by an eight-legged nymphal Amblyomma testudinarium. We re-emphasize the usefulness of dermoscopy for identifying signs of the bite and determining the species of the biting tick

Relationship Between Macrophage Differentiation And The Chemotactic Activity Toward Damaged Muscle Cells

Aim: We investigated the effect of macrophage differentiation on the chemotactic activity to invade local damaged muscle using in vitro models of muscle injury. Methods: C2C12 cell myoblasts, and J774 cell macrophages were used. The “killed-C2C12” cells were combined with live C2C12 cells (live:killed C2C12 = 1:0.5) as a partially damaged muscle model. The J774 cells were stimulated with LPS and DEX. The chemotactic activity of J774 cells was examined using TAXIScan device. Results: Although the velocity of J774 cells was little affected by each type of C2C12 cells (live, killed and combination), the directionality of the J774 cells was increased. The highest directionality of J774 cells was observed when the ratio of live-:killed-C2C12 cells was 1:0.5.The TLR4 and CD11c expressions of LPS cells were higher than those in both Ctrl and DEX cells. The LPS cells were strongly stained around the cell membrane by phalloidin, but the F-actin expression in DEX cells was in an orderly line along the long axis of cells. DEX cells showed stretching toward C2C12 cells, and their length/width ratio was higher than that in both Ctrl and LPS cells. Although the chemotactic activity of LPS cells disappeared completely, DEX cells exhibited accelerated chemotactic activity toward damaged muscle cells. The MCP-1 production in live-:killed-C2C12 cells was higher than that in the live-C2C12 cells. The CCR2 expression in DEX cells was higher than that in both Ctrl and LPS cells. Conclusion: Our conclusion is that: 1) the chemotactic activity of macrophages toward areas of damaged muscle induces more live myoblasts than damaged cells, 2) the chemotactic activity of macrophages is not due to velocity, but depends on the directionality toward damaged muscle cells, and 3) macrophage differentiation influences their chemotactic activity toward damaged muscle cells through the expression of CCR2 and/or F-actin

Transcriptional regulation of connective tissue growth factor by sphingosine 1-phosphate in rat cultured mesangial cells

AbstractConnective tissue growth factor (CTGF) is induced by transforming growth factor-β (TGF-β) via Smad activation in mesangial cells. We recently reported that sphingosine 1-phosphate (S1P) induces CTGF expression in rat cultured mesangial cells. However, the mechanism by which S1P induces CTGF expression is unknown. The present study revealed that S1P-induced CTGF expression is mediated via pertussis toxin-insensitive pathways, which are involved in the activation of small GTPases of the Rho family and protein kinase C. We also showed by luciferase reporter assays and chromatin immunoprecipitation that S1P induces CTGF expression via Smad activation as TGF-β does

Effects of chronic testosterone administration on the degree of preference for a high-fat diet and body weight in gonadal-intact and ovariectomized female rats

Energy balance and reproductive functions are closely linked in some species. The sex hormones (estrogens and androgens) are involved in the regulation of appetite, metabolism, body weight (BW), and body composition in mammals. Previously, we showed that the effects of testosterone on BW, appetite, and fat weight were markedly affected by alterations to the gonadal hormonal milieu. In this study, we examined whether testosterone administration changes food preferences and whether these effects of testosterone depend on gonadal status in female rats. We also evaluated the underlying mechanisms responsible for these effects, focusing on hypothalamic inflammation and endoplasmic reticulum (ER) stress. In gonadal-intact (sham) female rats, chronic testosterone administration promoted a preference for a high-fat diet (HFD) and increased BW gain, fat weight, and adipocyte size, whereas no such effects were observed in ovariectomized (OVX) rats. Testosterone administration increased hypothalamic interleukin-1 mRNA expression in the sham rats, but not the OVX rats. On the contrary, testosterone administration decreased the hypothalamic mRNA levels of ER stress-response genes in the OVX rats, but not the sham rats. These testosterone-induced alterations in OVX rats might represent a regulatory mechanism for preventing hypothalamic inflammation and the overconsumption of a HFD. In conclusion, testosterone’s effects on food preferences and the subsequent changes were affected by gonadal status. Testosterone-induced changes in hypothalamic inflammatory cytokine production and ER stress might be related to these findings

Effects of Low Energy Availability on Reproductive Functions and Their Underlying Neuroendocrine Mechanisms

It is known that metabolic disturbances suppress reproductive functions in females. The mechanisms underlying metabolic and nutritional effects on reproductive functions have been established based on a large body of clinical and experimental data. From the 1980s to 1990s, it was revealed that disrupted gonadotropin-releasing hormone (GnRH) secretion is the main cause of reproductive impairments in metabolic and nutritional disorders. From the late 1990s to early 2000s, it was demonstrated that, in addition to their primary functions, some appetite- or metabolism-regulating factors affect GnRH secretion. Furthermore, in the early 2000s, kisspeptin, which is a potent positive regulator of GnRH secretion, was newly discovered, and it has been revealed that kisspeptin integrates the effects of metabolic status on GnRH neurons. Recent studies have shown that kisspeptin mediates at least some of the effects of appetite- and metabolism-regulating factors on GnRH neurons. Thus, kisspeptin might be a useful clinical target for treatments aimed at restoring reproductive functions in individuals with metabolic or nutritional disturbances, such as those who exercise excessively, experience marked weight loss, or suffer from eating disorders. This paper presents a review of what is currently known about the effects of metabolic status on reproductive functions and their underlying mechanisms by summarizing the available evidence

Detection of quantitative trait loci controlling pre-harvest sprouting resistance by using backcrossed populations of japonica rice cultivars

Backcrossed inbred lines (BILs) and a set of reciprocal chromosome segment substitution lines (CSSLs) derived from crosses between japonica rice cultivars Nipponbare and Koshihikari were used to detect quantitative trait loci (QTLs) for pre-harvest sprouting resistance. In the BILs, we detected one QTL on chromosome 3 and one QTL on chromosome 12. The QTL on the short arm of chromosome 3 accounted for 45.0% of the phenotypic variance and the Nipponbare allele of the QTL increased germination percentage by 21.3%. In the CSSLs, we detected seven QTLs, which were located on chromosomes 2, 3 (two), 5, 8 and 11 (two). All Nipponbare alleles of the QTLs were associated with an increased rate of germination. The major QTL for pre-harvest sprouting resistance on the short arm of chromosome 3 was localized to a 474-kbp region in the Nipponbare genome by the SSR markers RM14240 and RM14275 by using 11 substitution lines to replace the different short chromosome segments on chromosome 3. This QTL co-localized with the low-temperature germinability gene qLTG3-1. The level of germinability under low temperature strongly correlated with the level of pre-harvest sprouting resistance in the substitution lines. Sequence analyses revealed a novel functional allele of qLTG3-1 in Nipponbare and a loss-of-function allele in Koshihikari. The allelic difference in qLTG3-1 between Nipponbare and Koshihikari is likely to be associated with differences in both pre-harvest sprouting resistance and low-temperature germinability

Heterogeneous Effects of Intensive Glycemic and Blood Pressure on Cardiovascular Events Among Diabetes by Living Arrangements

糖尿病患者における厳格な血糖・血圧管理の効果が、居住形態によって異なることが明らかに. 京都大学プレスリリース. 2024-07-03.Background: Although living alone versus with others is a key social element for cardiovascular prevention in diabetes, evidence is lacking about whether the benefit of intensive glycemic and blood pressure (BP) control differs by living arrangements. We thus aim to investigate heterogeneity in the joint effect of intensive glycemic and BP control on cardiovascular events by living arrangements among participants with diabetes. Methods and results: This study included 4731 participants with diabetes in the ACCORD-BP (Action to Control Cardiovascular Risk in Diabetes-Blood Pressure) trial. They were randomized into 4 study arms, each with glycated hemoglobin target (intensive, <6.0% versus standard, 7.0-7.9%) and systolic BP target (intensive, <120 mm Hg versus standard <140 mm Hg). Cox proportional hazard models were used to estimate the joint effect of intensive glycemic and BP control on the composite cardiovascular outcome according to living arrangements. At a mean follow-up of 4.7 years, the cardiovascular outcome was observed in 445 (9.4%) participants. Among participants living with others, intensive treatment for both glycemia and BP showed decreased risk of cardiovascular events compared with standard treatment (hazard ratio [HR], 0.68 [95% CI, 0.51-0.92]). However, this association was not found among participants living alone (HR, 0.96 [95% CI, 0.58-1.59]). P for interaction between intensive glycemic and BP control was 0.53 among participants living with others and 0.009 among those living alone (P value for 3-way interaction including living arrangements was 0.049). Conclusions: We found benefits of combining intensive glycemic and BP control for cardiovascular outcomes among participants living with others but not among those living alone. Our study highlights the critical role of living arrangements in intensive care among patients with diabetes