Many studies revealed the potential of honey consumption in controlling obesity. However, no study has been conducted using Malaysian honey. In this study, we investigated the efficacy of two local Malaysian honey types: Gelam and Acacia honey in reducing excess weight gain and other parameters related to obesity. The quality of both honey types was determined through physicochemical analysis and contents of phenolic and flavonoid. Male Sprague-Dawley rats were induced to become obese using high fat diet (HFD) prior to introduction with/without honey or orlistat for four weeks. Significant reductions in excess weight gain and adiposity index were observed in rats fed with Gelam honey compared to HFD rats. Moreover, levels of plasma glucose, triglycerides, and cholesterol, plasma leptin and resistin, liver enzymes, renal function test, and relative organ weight in Gelam and Acacia honey treated groups were reduced significantly when compared to rats fed with HFD only. Similar results were also displayed in rats treated with orlistat, but with hepatotoxicity effects. In conclusion, consumption of honey can be used to control obesity by regulating lipid metabolism and appears to be more effective than orlistat.
Honey authenticity is one of the most critical honey trading issues worldwide. Fake honey (FH) represents almost 80% of the honey market in Malaysia. Apart from violating consumer’s rights, FH consists of none of the beneficial nutritional value other than pure honey (PH). Moreover, prolonged consumption of FH may cause harm to human health. However, data regarding these issues is limited. In this study, both PH and FH were tested using 3T3-L1 adipocytes and in high-fat diet (HFD)-induced obese Sprague Dawley rats. Initially, a physicochemical analysis was performed on both the honey samples according to the Codex Alimentarius Commission and International Honey Commission procedures. After 72 hr, PH significantly reduced lipid accumulation and triglyceride levels in the adipocytes. In the rats, low glucose, cholesterol, and triglyceride levels were significantly detected after orally administered for 16 weeks. Conversely, FH significantly induced higher lipid accumulation and triglyceride levels in adipocytes and excess high blood glucose, cholesterol, and triglyceride levels in rats. The results demonstrated that FH has negative effects on lipid metabolism, and prolonged consumption may cause health complications. Furthermore, prompt actions are required to address this problem.
Background Hepatocellular carcinoma (HCC) has become a prominent global health threat due to its occurrence, lethality and dismal survival rates. Increasing prevalence of obesity and diabetes-induced non-alcoholic fatty liver disease (NAFLD) and metabolic syndromes have been found culpable for the rise of HCC initiation, via disruption of liver microenvironment. Super enhancers, which are characterised by high density of transcription binding sites, high-level transcription regulation and response to external stimulation, determine cell fate during oncogenesis. Master transcription factors translate microenvironmental changes into super enhancer remodelling and activation, which subsequently changes the gene expression profile and define cell identity. This project aims at profiling the super enhancer status in the context of NAFLD-associated HCC and to unveil the master transcription factors responsible for dietinduced HCC progression. Methods Nanoscale chromatin immunoprecipitation sequencing (nano ChIP-seq) against histone marks H3K27ac, H3K4me1 and H3K4me3 in 6 pairs of primary human NAFLD-HCC tumours and their adjacent non-tumour tissues revealed potential oncogenic super enhancers. Global mRNA expression was detected by RNA sequencing (RNA-seq) to support the enhancer-target gene transcription axis. Master transcription factor regulation of NAFLD-HCC super-enhancers was further supported by integrated bioinformatics analysis, including motif enrichment and signature transcription factor discovery. ChIP-seq data for the master transcription factors in HepG2 cells confirmed their occupancies on super enhancers controlling key oncogenic pathways. Results Tumor-enabling super enhancers (averaged 553 and 484 per HCC tumour and non-tumour tissue, respectively) were profiled in primary human NAFLD-HCC tissues, and master transcription factors showed significant binding to NAFLD-HCC oncogenic super enhancers. Interestingly, tumorenabling super enhancers co-bound by HCC-specific master transcription factors target critical genes involved in hepatic inflammation and NAFLD pathogenesis. Conclusions Integrated analysis of chromatin profiling and transcriptome in primary human tissues provides insights into the trans-regulatory network involving oncogenic super enhancers and master transcription factors during the pathogenic process of metabolic syndrome-associated HCC.
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