Long intergenic noncoding RNAs (lincRNAs) have a variety of properties that differ from those of messenger RNAs (mRNAs) encoding proteins. Long intergenic nonprotein coding RNA 667 (LINC00667) is a non-coding transcript located on chromosome 18p11.31. Recently, many studies have found that LINC00667 can enhance the progression of various cancers and play a key part in a lot of diseases, such as tumorigenesis. Therefore, LINC00667 can be recognized as a potential biomarker and therapeutic target. So, we reviewed the biological functions, relevant mechanisms, as well as clinical significance of LINC00667 in several human cancers in detail.

Aging is a growing trend in modern societies, and the incidence of aging-related obesity has been on a steady rise. The key cause of obesity of older adults is identified as the decreased lipolysis of adipocytes, which in turn can be attributed to the decreased expression of key lipases in senescent adipocytes, but effective clinical measures to enhance the lipase expression are currently lacking. In this work, we studied the influence of the total saponins from Panax japonicus (TSPJs) on the expression of key lipases in senescent adipocytes, which can provide an experimental basis for potentially using TSPJs to address aging-related obesity. We found that TSPJs could regulate lipase expression through the ALK7-SMADs signaling pathway, to restore the lipase expression in senescent adipocytes and thus improve lipolysis.

Adipocytic lipolysis is strongly related to the increase of visceral fat, decrease of exercise capacity, and various other metabolic syndromes during aging. It is significantly influenced by the paracrine relationship between adipocytes and the adipose tissue macrophages (ATMs), and the cytokines secreted by ATMs have endocrine effects on adjacent tissues. We previously reported that the total saponins from Panax japonicus (TSPJs) can enhance lipid metabolism. In this work, we for the first time proved that TSPJs promoted adipocytic lipolysis by preventing NLRP3 activation in ATMs to inhibit the expression of GDF3. The decrease of GDF3 by TSPJs restored the expression of the adipose triglyceride lipase (ATGL) and phosphorylated hormone-sensitive lipase (p-HSL), both of which are known to decrease with aging. Thus, the NLRP3 inflammasome/GDF3/ATGL axis may be a worthy target in developing future clinical solutions for aging-related obesity.

ABSTRACTBalanophora harlandiiHook (B. harlandii), a folk medicine, has been traditionally employed to treat traumatic bleeding, gastroenteritis, icteric hepatitis, hemorrhoids, and other conditions. In this work, polysaccharides with anti-inflammatory effects were extracted and purified fromB. harlandii.The extraction conditions were optimized, and the properties of one purified neutral fraction, denoted as BHPs-W-S3, were analyzed. Gel permeation chromatography (GPC) was carried out to measure the molecular weight. The structure of BHPs-W-S3 was assessed based on monosaccharide composition analysis, Fourier transform infrared (FT-IR) spectroscopy, methylation analysis, and nuclear magnetic resonance (NMR) spectroscopy. BHPs-W-S3 has a molecular weight of 14.1 kDa, and its three main monosaccharides are glucose, galactose, and mannose with a molar ratio of 6.4:1.7:1.1. Its main chain consists of →6)-α-D-Glcp-(1→, →4,6)-α-D-Glcp-(1→, →6)-β-D-Galp-(1→, →3,6)-β-D-Galp-(1→, and it has branch chains at the O-4 and/or O-3 positions. In addition,in vitroexperiments show that the polysaccharides fromB. harlandican decrease the phosphorylation level of p65 and IKB-α in LPS-induced RAW264.7 cells to reduce the expression of the pro-inflammatory genes such as TNF-α, IL-6, and IL-1β.Abstract Figure

Balanophora harlandii Hook ( B. harlandii) , a folk medicine, has been traditionally employed to treat traumatic bleeding, gastroenteritis, icteric hepatitis, hemorrhoids, and other conditions. In this work, polysaccharides with anti-inflammatory effects were extracted and purified from B. harlandii. The extraction conditions were optimized, and the properties of one purified neutral fraction, denoted as BHPs-W-S3, were analyzed. Gel permeation chromatography (GPC) was carried out to measure the molecular weight. The structure of BHPs-W-S3 was assessed based on monosaccharide composition analysis, Fourier transform infrared (FT-IR) spectroscopy, methylation analysis, and nuclear magnetic resonance (NMR) spectroscopy. BHPs-W-S3 has a molecular weight of 14.1 kDa, and its three main monosaccharides are glucose, galactose, and mannose with a molar ratio of 6.4:1.7:1.1. Its main chain consists of →6)-α-D-Glcp-(1→, →4,6)-α-D-Glcp-(1→, →6)-β-D-Galp-(1→, →3,6)-β-D-Galp-(1→, and it has branch chains at the O-4 and/or O-3 positions. In addition, in vitro experiments show that the polysaccharides from B. harlandi can decrease the phosphorylation level of p65 and IKB-α in LPS-induced RAW264.7 cells to reduce the expression of the pro-inflammatory genes such as TNF-α, IL-6, and IL-1β. ![Figure][1] * ### Abbreviations Ara : arabinose B. harlandii : Balanophora harlandii Hook BHPs : B. harlandii polysaccharides BHPs-W-S3 : a neutral polysaccharide of B. harlandii polysaccharides BSA : bovine serum albumin DEX : Dexamethasone Fru : Fructose Fuc : Fucose FT-IR : Fourier transform infrared spectroscopy GalA : Galacturonic acid GC-MS : gas chromatography-mass spectrometry GlcN : Gal galactose GlcN : Glucosamine hydrochloride GlcA : Glucuronic acid GlcNC : N-Acetyl-D glucosamine Glc : glucose GulA : Gullochuronic acid GPC : gel permeation chromatography IκBα : inhibitor of kappa Bα LPS : lipopolysaccharide ManA : Mannuronic acid Man : mannose NMR : nuclear magnetic resonance NFκB : Nuclear factor kappa-B PI : polydispersity index PVDF : polyvinylidene difluoride PBS : phosphate-buffered saline p-IκBα : phospho-inhibitor of kappa Bα Rha : Rhamnose Rib : Ribose SD : standard deviation SAR : structure-activity relationship TBS-Tween : Tris-buffered saline-Tween TFA : trifluoroacetic acid TBS-Tween : Tris-buffered saline-Tween UV : ultraviolet Xyl : Xylose [1]: pending:yes

Aging and obesity are closely related, and the prevalence of obesity and metabolic diseases are rapidly increasing with an aging population worldwide. A key change in the adipose tissue during the aging process is the decline of lipolysis, and the excitation of the sympathetic nerve system is a key pathway to promote lipolysis. Previous studies have shown that the total saponins from Panax japonicus (TSPJs) can prevent obesity in mice with high-fat diet by increasing fat decomposition. In this work, we examine the regulatory effects of TSPJs on lipolysis in the aging state and explore the possible mechanisms. TSPJs can promote the excitation of sympathetic nerves by increasing the expression of tyrosine hydroxylase in the adipose tissue, which positively regulates the expression of lipases to revitalize lipolysis. The results suggest that TSPJs can help to resist aging-induced obesity and may be a potential medication for weight management.

As the living standards of people are increasingly improved, obesity has become a hotspot in our daily life. Obesity has been found as a chronic and recurrent disease with serious adverse consequences. Over the past few years, several articles indicated that long non-coding RNA taurine increased gene 1 (lncRNA TUG1), a useful RNA, which was indicated to show a relationship to obesity-related disease occurrence and development. Exosomes are recognized as an emerging research field that includes substances actively involved in regulating the molecular mechanisms of disease. This review summarizes the current relevant TUG1 in different molecular pathways of obesity-associated diseases, the correlation between exosomes and TUG1, or obesity-associated diseases. The aim is to explore TUG1 as a novel target for obesity, which can deepen the knowledge regarding the epigenetic regulation pathway. Furthermore, it is expected to focus on diseases associated with obesity treatment and diagnosis.

Aging refers to a natural process and a universal phenomenon in all cells, tissues, organs, and the whole organism. Long non-coding RNAs (lncRNAs) are non-coding RNAs with a length of 200 nucleotides. LncRNA growth arrest-specific 5 (lncRNA GAS5) is often down-regulated in cancer. The accumulation of lncRNA GAS5 has been found to be able to inhibit cancer growth, invasion, and metastasis while enhancing the sensitivity of cells to chemotherapy drugs. LncRNA GAS5 can be a signaling protein, which is specifically transcribed under different triggering conditions. Subsequently, it is involved in signal transmission in numerous pathways as a signal node. LncRNA GAS5, with a close relationship to multiple miRNAs, was suggested to be involved in the signaling pathway under three action modes (i.e., signal, bait, and guidance). LncRNA GAS5 was found to be involved in different age-related diseases (e.g., rheumatoid arthritis, type 2 diabetes, atherosclerosis, osteoarthritis, osteoporosis, multiple sclerosis, cancer, etc.). This study mainly summarized the regulatory effect exerted by lncRNA GAS5 on age-related diseases.

Background: Increasing academic efforts have been made to explore the correlation of long noncoding RNAs (lncRNAs) with human diseases, particularly metabolic diseases like diabetes mellitus. Taking lncRNA H19 as an example, this review intends to reveal the functions and mechanism of lncRNA H19 in diabetes mellitus and diabetic complications. Methods: The research results associated with lncRNA H19 and diabetes mellitus are collected and summarized on PubMed. Conclusion: LncRNA H19 is a potential instructive marker for the treatment of diabetes mellitus and diabetic complications.

With the continuous improvement of living standards, obesity has become an inevitable hotspot in our daily life. It remains a chronic and recurrent disease with serious adverse consequences. Over the past few years, several articles suggested that long non-coding RNA taurine increased gene 1（lncRNA TUG1）, a useful RNA, was suggested to show a relationship to obesity-related disease occurrence and development. Exosome is an emerging research field, which contains substances that are actively involved in regulating the molecular mechanisms of disease. This review summarizes the current relevant TUG1 in different molecular pathways of diseases related to obesity, relationship between exosomes and TUG1 or diseases related to obesity. The aim is to explore TUG1 as a novel target for obesity, which can deepen the knowledge regarding epigenetic regulation pathway. Besides, it is likely to be a potential future targeting diseases related to obesity site treatment and diagnosis.

BACKGROUND:Nuclear-enriched abundant transcript 1 (abbreviated as NEAT1) is a long-chain noncoding RNA involved in various physiological and pathological processes. This study aimed to clarify the effect and molecule system of NEAT1 within non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes (T2DM). METHODS:In this review, current studies concerning mechanisms of NEAT1l, in the development of type 2 diabetes and its complications have been summarized and analyzed. Also, we searched the papers based on NEAT1 related to NAFLD. The related studies were obtained through a systematic search of Pubmed. RESULTS:NEAT1 displays a close correlation with how T2DM occurs and develops, and it was confirmed to be significantly up-regulated in T2DM and its various complications (e.g., diabetics nephropathy, diabetics cardiomyopathy, diabetics retinopathy as well as diabetic neuropathy). Besides, NEAT1 is capable of impacting the occurrence, development and prognosis of NAFLD and T2DM. CONCLUSION:LncRNA NEAT1 is likely to act as a novel therapeutic target for T2DM and its complications. Moreover, non-alcoholic fatty liver disease is also correlated with NEAT1.

Astragaloside IV (AST) is a major bioactive compound of Radix Astragali with medical and health benefits. Previous studies have found that AST can reduce the body weights of high-fat diet fed mice. However, the effect of AST on fat metabolism of ageing mice is unclear. In this study, naturally ageing mice were administered intragastrically with AST at 30 mg/kg/day (ageing + AST-L group) and 90 mg/kg/day (ageing + AST-H group) for 16-20 months. Adult (4 months old) and ageing mice were given 1% sodium carboxyl methylcellulose as vehicle. Energy metabolism-related biological parameters of living mice were examined. Moreover, mRNA and protein levels of key enzymes/proteins involved in triglyceride (TG) lipolysis, fatty acid β-oxidation (FAO), ketone body (KB) production and mitochondrial respiratory chain were also examined after sacrifice. Results demonstrated that treatment with AST significantly reduced body weight, white fat and liver/body weight ratio of ageing mice, significantly reduced serum/hepatic TG levels, respiratory quotient, promoted fatty acid mobilization in white adipose tissue, mitochondrial FAO and KB production and mitochondrial biosynthesis/functions in the liver of ageing mice. AST also up-regulated the expression of phosphorylated AMP-activated protein kinase, acetyl-CoA carboxylase, acetyl-coenzyme A synthetase, carnitine palmitoyltransferase 1a/1b, enoyl coenzyme A hydratase-short chain, acyl-CoA dehydrogenase medium chain and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase-2 involved in fat metabolism. These results indicated that mitochondrial activity could be the target of AST to treat abnormal fat metabolism during ageing.

Long non-coding RNAs (lncRNAs) exhibit a length more than 200 nucleotides and they are characterized by non-coding RNAs (ncRNA) not encoded into proteins. Over the past few years, the role and development of lncRNAs have aroused the rising attention of researchers. To be specific, KCNQ1OT1, the KCNQ1 opposite strand/antisense transcript 1, is clearly classified as a regulatory ncRNA. KCNQ1OT1 is capable of interacting with miRNAs, RNAs and proteins, thereby affecting gene expression and various cell functions (e.g., cell proliferation, migration, epithelial–mesenchymal transition (EMT), apoptosis, viability, autophagy and inflammation). KCNQ1OT1 is dysregulated in a wide range of human diseases (e.g., cardiovascular disease, cancer, diabetes, osteoarthritis, osteoporosis and cataract), and it is speculated to act as a therapeutic target for treating various human diseases. On the whole, this review aims to explore the biological functions, underlying mechanisms and pathogenic roles of KCNQ1OT1 in human diseases.

Lipid metabolism disorder is a multifactor issue, which contributes to several serious health consequences, such as obesity, hyperlipidemia, atherosclerosis diabetes, non-alcoholic fatty liver, etc. Tannins, applied as naturally derived plants, are commonly used in the study of lipid metabolism disease with excellent safety and effectiveness while producing less toxic and side effects. Meanwhile, recognition of the significance of dietary tannins in lipid metabolism disease prevention has increased. As suggested by existing evidence, dietary tannins can reduce lipid accumulation, block adipocyte differentiation, enhance antioxidant capacity, increase the content of short-chain fatty acids, and lower blood lipid levels, thus alleviating lipid metabolism disorder. This study is purposed to sum up and analyze plenty of documents on tannins, so as to provide the information required to assess the lipid metabolism of tannins.