Response of gut microbiota and inflammatory status to bitter melon (Momordica charantia L.) in high fat diet induced obese rats

Ethnopharmacological relevance: Bitter melon (Momordica charantia L.) is rich in a variety of biologically active ingredients, and has been widely used in traditional Chinese medicine (TCM) to treat various diseases, including type 2 diabetes and obesity. Aim of the study: We aimed to investigate how bitter melon powder (BMP) could affect obesity-associated inflammatory responses to ameliorate high-fat diet (HFD)-induced insulin resistance, and investigated whether its anti-inflammatory properties were effected by modulating the gut microbiota. Materials and methods: Obese SD rats (Sprague-Dawley rats, rattus norregicus) were randomly divided into four groups: (a) normal control diet (NCD) and distilled water, (b) HFD and distilled water, (c) HFD and 300 mg BMP/kg body weight (bw), (d) HFD and 10 mg pioglitazone (PGT)/kg bw. Results: We observed remarkable decreases in the fasting glucose, fasting insulin, HOMA-IR index, serum lipid levels, and cell sizes of epididymal adipose tissues in the BMP and PGT groups after 8 weeks. BMP could significantly improve the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), anti-inflammatory cytokine interleuldn-10 (IL-10), and local endotoxin levels compared to the HFD group (p < 0.05). BMP suppressed the activation of nuclear factor-kappa B (NF-kappa B) by inhibiting inhibitor of NF-kappa B alpha (I kappa B alpha) degradation and phosphorylation of c-Jun N-terminal kinase/ p38 mitogen-activated protein kinases (JNK/p38 MAPKs) in adipose tissue. Sequencing results illustrated that BMP treatment markedly decreased the proportion of the endotoxin-producing opportunistic pathogens and increased butyrate producers. Conclusions: These results demonstrate that BMP ameliorates insulin sensitivity partly via relieving the inflammatory status in the system and in white adipose tissues of obese rats, and is associated with a proportional regulation of specific gut microbiota.