Resistant starch from green banana (Musa sp.) attenuates non-alcoholic fat liver accumulation and increases short-chain fatty acids production in high-fat diet-induced obesity in mice

• Published in: International journal of biological macromolecules Vol. 145; pp. 1066 - 1072
• Main Authors: Rosado, Carolyne Pimentel, Rosa, Victor Hugo Cordeiro, Martins, Bruna Cadete, Soares, Aruanna Cajaty, Santos, Izabelle Barcellos, Monteiro, Elisa Bernardes, Moura-Nunes, Nathália, da Costa, Cristiane Aguiar, Mulder, Alessandra da Rocha Pinheiro, Daleprane, Julio Beltrame
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15-02-2020
• Subjects: Animals; Diet, High-Fat - adverse effects; Dietary Carbohydrates - therapeutic use; Dietary Supplements; Disease Models, Animal; Eating; Fasting; Fatty Acids, Volatile - metabolism; Glucose - metabolism; Glucose Tolerance Test; Insulin; Lipid Metabolism - drug effects; Liver - drug effects; Liver - metabolism; Liver - pathology; Male; Metabolism; Mice; Mice, Inbred C57BL; Musa - chemistry; Non-alcoholic Fatty Liver Disease - metabolism; Obesity; Obesity - metabolism; Plant Extracts - pharmacology; Resistant starch; Starch - administration & dosage; Steatosis; Triglycerides - metabolism; Obesity; Resistant starch; Metabolism; Insulin; Steatosis
• ISSN: 0141-8130; 1879-0003
• DOI: 10.1016/j.ijbiomac.2019.09.199

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•Green banana is a source of resistant starch.•Resistant starch from green banana regulates glucose metabolism in high-fat fed-mice.•Resistant starch from green banana increase short chain fatty acid production and regulate lipid metabolism.
This study aimed to investigate the effect of resistant starch from green banana (GB) on steatosis and short-chain fatty acid (SCFAs) production in high fat diet-induced obesity in mice. High-fat green banana group (HFB) exhibited lower gains in BM (body mass; −6%; P < 0.01) compared with High-fat diet group (HF). Additionally, HFB mice showed reduction in liver steatosis (−28%, P < 0.01) with reduction of 93% in hepatic triacylglycerol (P < 0.01) compared to HF-diet-fed mice. In addition, the protein abundance of AMPKp/AMPK, HMGCoA-r and FAS were downregulated in livers of HFB mice (P < 0.01), relatively to the HF-diet-fed mice. ABCG8 and ABCG5 were up-regulated in HFB group compared to HF group (P < 0.01). Furthermore, the HFB fed-mice produced the highest amount of SCFAs (p < 0.05) compared to its counterpart HFD. In conclusion, we demonstrated that resistant starch from GB improved metabolic parameters by modulating the expression of key proteins involved in liver lipid metabolism.