Low-level of chronic inflammation activation is characteristic of obesity. Nonalcoholic fatty liver disease (NAFLD) is closely linked to obesity and is an emerging health problem, it originates from abnormal accumulation of triglycerides in the liver, and sometimes causes inflammatory reactions that could contribute to cirrhosis and liver cancer, thus its pathogenesis needs to be clarified for more treatment options. Once NAFLD is established, it contributes to systemic inflammation, the low-grade inflammation is continuously maintained during NAFLD causing impaired resolution of inflammation in obesity, which subsequently exacerbates its severity. This study focuses on the effects of obesity-induced inflammations, which are the underlying causes of the disease progression and development of more severe inflammatory and fibrotic stages. Understanding the relationship between obesity and NAFLD could help in establishing attractive therapeutic targets or diagnostic markers in obesity-induced inflammation response and provides new approaches for the prevention and treatment of NAFLD in obesity.

Inflammation initiates a vicious cycle between obesity and nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a new challenge in modern medicine, due to its high prevalence in the world. The pathogenesis of NAFLD is a complex dysmetabolic process, following the “multiple-hit” hypothesis that involves hepatocytes excessive accumulation of triglycerides, insulin resistance (IR), increased oxidative stress, chronic low-grade inflammatory response and lipotoxicity. In this review, we provide an overview of the interrelation of these processes, the link between systemic and local inflammation and the role of dysfunctional adipose tissue (AT) in the NAFLD development. Multiple extrahepatic triggers of the pathophysiological mechanisms of NAFLD are described: nutritional deficiency or malnutrition, unhealthy food intake, the dysfunction of the liver–gut axis, the involvement of the mesenteric adipose tissue, the role of adipokines such as adiponectin, of food intake hormone, the leptin and leptin resistance (LR) and adipose tissue’s hormone, the resistin. In addition, a wide range of intrahepatic players are involved: oxidative stress, fatty acid oxidation, endoplasmic reticulum stress, mitochondrial dysfunction, resident macrophages (Kupffer cells), neutrophils, dendritic cells (DCs), B and T lymphocytes contributing to the potential evolution of NAFLD to nonalcoholic steatohepatitis (NASH). This interdependent approach to complex dysmetabolic imbalance in NAFLD, integrating relevant studies, could contribute to a better clarification of pathogenesis and consequently the development of new personalized treatments, targeting de novo lipogenesis, chronic inflammation and fibrosis. Further studies are needed to focus not only on treatment, but also on prevention strategy in NAFLD.

/pdf/chronic-inflammation-a-link-between-nonalcoholic-fatty-liver-1eoio6xc.pdf

Chronic Inflammation—A Link between Nonalcoholic Fatty Liver Disease (NAFLD) and Dysfunctional Adipose Tissue

Polymers show a vast possibility of chemical modification of novel properties and nanomedicine generation in biomedical fields. Polymeric nanoparticle (PNPs) is commonly used as a drug carrier, they have good biodegradability, biocompatibility, and high drug-loading capacity. PNPs are the broadly used nanocarrier including polymeric micelles, liposomes, dendrimers, polymeric sponges, and colloidal carriers. These NPs also show low toxicity, increased therapeutic effectiveness, improved drug penetration, controlled drug release and enhanced physical and chemical stability. PNPs are widely used as a drug delivery system subsequently they are able to load natural and synthetic agents including, protein, peptides, growth factors, DNAs, mRNA, and drugs. PNPs can be applied via several routes of administration as nasal, oral, intravenous, topical and ocular. PNPs can potentially target specific cells/tissues, NPs are a promising way to increase local drug concentration, decrease toxicity and side effects, and prevent nonspecific interaction. The present review focuses on biodegradable polymers, classifications, PNPs types, method and preparation of PNPs, and biomedical applications in targeted drug delivery and their limitations. This review presents targeted drug delivery for respiratory, cancers, liver cirrhosis, ocular, diabetic wounds, and Alzheimer's disease. 

Current updated review on preparation of polymeric nanoparticles for drug delivery and biomedical applications

Luteolin is a flavonoid widely present in various traditional Chinese medicines. In recent years, luteolin has received more attention due to its impressive liver protective effect, such as metabolic associated fatty liver disease, hepatic fibrosis and hepatoma. This article summarizes the pharmacological effects, pharmacokinetic characteristics, and toxicity of luteolin against liver diseases, and provides prospect. The results indicate that luteolin improves liver lesions through various mechanisms, including inhibiting inflammatory factors, reducing oxidative stress, regulating lipid balance, slowing down excessive aggregation of extracellular matrix, inducing apoptosis and autophagy of liver cancer cells. Pharmacokinetics research manifested that due to metabolic effects, the bioavailability of luteolin is relatively low. It is worth noting that appropriate modification, new delivery systems, and derivatives can enhance its bioavailability. Although many studies have shown that the toxicity of luteolin is minimal, strict toxicity experiments are still needed to evaluate its safety and promote its reasonable development. In addition, this study also discussed the clinical applications related to luteolin, indicating that it is a key component of commonly used liver protective drugs in clinical practice. In view of its excellent pharmacological effects, luteolin is expected to become a potential drug for the treatment of various liver diseases. 

Luteolin as a potential hepatoprotective drug: Molecular mechanisms and treatment strategies.

Ghrelin is the only known orexigenic gut hormone, and its synthesis, secretion and degradation are affected by different metabolic statuses. This meta-analysis aimed to investigate the potential differences in plasma acyl ghrelin (AG) and des-acyl ghrelin (DAG) concentrations between normal weight and obese adults. Systematic literature searches of PubMed, Embase and Web of Science through October 2021 were conducted for articles reporting AG or DAG levels in obesity and normal weight, and 34 studies with 1863 participants who met the eligibility criteria were identified. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated to evaluate group differences in circulating AG and DAG levels. Pooled effect size showed significantly lower levels of baseline AG (SMD: - 0.85; 95% CI: - 1.13 to - 0.57; PSMD < 0.001) and DAG (SMD: - 1.06; 95% CI: - 1.43 to - 0.69; PSMD < 0.001) in obese groups compared with healthy controls, and similar results were observed when subgroup analyses were stratified by the assay technique or storage procedure. Postprandial AG levels in obese subjects were significantly lower than those in controls when stratified by different time points (SMD 30 min: - 0.85, 95% CI: - 1.18 to - 0.53, PSMD < 0.001; SMD 60 min: - 1.00, 95% CI: - 1.37 to - 0.63, PSMD < 0.001; SMD 120 min: - 1.21, 95% CI: - 1.59 to - 0.83, PSMD < 0.001). In healthy subjects, a postprandial decline in AG was observed at 120 min (SMD: - 0.42; 95% CI: - 0.77 to - 0.06; PSMD = 0.021) but not in obese subjects (SMD: - 0.28; 95% CI: - 0.60 to 0.03; PSMD = 0.074). The mean change in AG concentration was similar in both the obese and lean health groups at each time point (ΔSMD30min: 0.31, 95% CI: - 0.35 to 0.97, PSMD = 0.359; ΔSMD60min: 0.17, 95% CI: - 0.12 to 0.46, PSMD = 0.246; ΔSMD120min: 0.21, 95% CI: - 0.13 to 0.54, PSMD = 0.224). This meta-analysis strengthens the clinical evidence supporting the following: lower baseline levels of circulating AG and DAG in obese individuals; declines in postprandial circulating AG levels, both for the healthy and obese individuals; a shorter duration of AG suppression in obese subjects after meal intake. These conclusions have significance for follow-up studies to elucidate the role of various ghrelin forms in energy homeostasis. 

/pdf/circulating-acyl-and-des-acyl-ghrelin-levels-in-obese-adults-669lpmq7.pdf

Circulating acyl and des-acyl ghrelin levels in obese adults: a systematic review and meta-analysis

Luteolin alleviates non-alcoholic fatty liver disease in rats via restoration of intestinal mucosal barrier damage and microbiota imbalance involving in gut-liver axis

Luteolin (Lu) is a kind of flavonoid that has been proved to treat non-alcoholic fatty liver disease by alleviating intestinal microbiota disorder. In this study, luteolin was coated with methoxy poly(ethylene glycol)–poly(dl-lactide-co-glycolic acid) (mPEG-PLGA) using an emulsion solvent evaporation method, and the optimum preparation process was determined by a single-factor experiment combined with response surface methodology (RSM). Methacrylic acid-methyl methacrylate (1:2) copolymer (Eudragit S100) was then used to coat the surface of Lu/mPEG-PLGA nanoparticles. The physical parameters of Eudragit S100-coated Lu/mPEG-PLGA nanoparticles (Lu-NPs), such as appearance, particle size, potential, particle size distribution and drug release, and stability in vitro, were evaluated. In addition, its cytotoxicity in vitro, pharmacokinetics, tissue distribution, and toxicity in vivo were also studied. The results showed that the prepared Lu-NPs had uniform particle size distribution, high encapsulation efficiency, and good stability. Normal colonic epithelial cells showed good tolerance to Lu-NPs. After oral administration, the blood concentration of luteolin peaked at 8 h, and the main tissue distribution was within the colon, confirming its colon-targeted profile. Safety assessments also indicated that no significant changes were observed in main organs after administration of Lu-NPs. The use of Eudragit S100-coated Lu/mPEG-PLGA nanoparticles is a new strategy for colon-targeted delivery of luteolin that encourages luteolin to fulfill its role in the colon.

Development, Characterization, and Investigation of In Vivo Targeted Delivery Efficacy of Luteolin-Loaded, Eudragit S100-Coated mPEG-PLGA Nanoparticles

Objective(s): Ghrelin is a brain-gut peptide involved in substance and energy metabolism To confirm the hypothesis that ghrelin might be involved in non-alcoholic fatty liver disease (NAFLD), a rat NAFLD model was established and the changes of ghrelin were exploredMaterials and Methods: The rats were divided into control and NAFLD groups The rats in the NAFLD group were fed a high-fat–high-cholesterol (HFHC) diet for 8 weeks Total ghrelin (TG), acylated ghrelin (AG), unacylated ghrelin (UAG), and hypothalamic AG and its receptor GHSR-1a expression were detected using ELISA, RIA, RT-PCR, and Western blot, respectivelyResults: Plasma UAG, TG, and the ratio of UAG to AG (UAG/AG) decreased, while protein and mRNA expression of hypothalamic AG and growth hormone secretagogue receptor-1a (GHSR-1a) increased in NAFLD (P<001) Plasma UAG and UAG/AG were negatively associated with homeostatic model assessment insulin resistance (HOMA-IR), while AG positively correlated with HOMA-IR (R2=06510, P=0005; R2=08520, P=0000; R2=05617, P=0013, respectively) Plasma UAG, TG and UAG/AG negatively correlated with serum LDL-C or hepatic triglycerides (TGs) (R2=07733, P=0001; R2=06930, P=0003; R2=06042, P=0008; R2=07046, P=0002; R2=06722, P=0004; R2=05124, P=0020, respectively) Hypothalamic AG and GHSR-1a positively correlated with HOMA-IR or hepatic TGs (R2=05116, P=0020; R2=05220, P=0018; R2=06074, P=0008; R2=05127, P=0020, respectively)Conclusion: It might be that decreased circulating UAG/AG, rather than UAG or AG alone, were involved in IR and liver lipid accumulation in NAFLD Acylated ghrelin might induce IR and promote liver lipid accumulation via a central mechanism involved in the hypothalamus

https://ijbms.mums.ac.ir/article_15984_f900161c214b3e7a1ee35f0b2a2e142a.pdf

The role of acylated ghrelin and unacylated ghrelin in the blood and hypothalamus and their interaction with nonalcoholic fatty liver disease.

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Luteolin alleviates non-alcoholic fatty liver disease in rats via restoration of intestinal mucosal barrier damage and microbiota imbalance involving in gut-liver axis

Development, Characterization, and Investigation of In Vivo Targeted Delivery Efficacy of Luteolin-Loaded, Eudragit S100-Coated mPEG-PLGA Nanoparticles

The role of acylated ghrelin and unacylated ghrelin in the blood and hypothalamus and their interaction with nonalcoholic fatty liver disease.