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      Mulberry leaf polysaccharides ameliorate obesity through activation of brown adipose tissue and modulation of the gut microbiota in high-fat diet fed mice

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          Abstract

          Mulberry leaf polysaccharides have anti-obesity effects, and their mechanism likely involves an integrated role of white adipose browning, BAT activity induction and gut microbiota modulation.

          Abstract

          Improving energy homeostasis and the gut microbiota is a promising strategy to improve obesity and related metabolic disorders. Mulberry leaf is one of the traditional Chinese medicines and functional diets. In this work, a mouse model induced by high-fat diet (HFD) was used to reveal the role of mulberry leaf polysaccharides (MLP). It was found that MLP had a significant effect in limiting body weight gain (reduced by 19.95%, 35.47% and 52.46%, respectively), ameliorating hepatic steatosis and regulating lipid metabolism in HFD induced obese mice ( P < 0.05). RT-PCR and western blot analysis suggested that these metabolic improvements were mediated by inducing the development of brown-like adipocytes in inguinal white adipose tissue and enhancing brown adipose tissue activity. Besides, 16S rRNA sequencing results led to the inference that MLP could mitigate the composition and function of the gut microbiota. Together, these findings indicated that MLP possess great potential as a diet supplement or medication for obesity.

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          Most cited references39

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          Brown adipose tissue: function and physiological significance.

          The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogenesis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.
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            Functional interactions between the gut microbiota and host metabolism.

            The link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease.
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              Gut microbiota from twins discordant for obesity modulate metabolism in mice.

              The role of specific gut microbes in shaping body composition remains unclear. We transplanted fecal microbiota from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the U.S. diet. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes, were transmissible with uncultured fecal communities and with their corresponding fecal bacterial culture collections. Cohousing mice harboring an obese twin's microbiota (Ob) with mice containing the lean co-twin's microbiota (Ln) prevented the development of increased body mass and obesity-associated metabolic phenotypes in Ob cage mates. Rescue correlated with invasion of specific members of Bacteroidetes from the Ln microbiota into Ob microbiota and was diet-dependent. These findings reveal transmissible, rapid, and modifiable effects of diet-by-microbiota interactions.
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                Author and article information

                Contributors
                Journal
                FFOUAI
                Food & Function
                Food Funct.
                Royal Society of Chemistry (RSC)
                2042-6496
                2042-650X
                January 24 2022
                2022
                : 13
                : 2
                : 561-573
                Affiliations
                [1 ]Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, 300072, P. R. China
                [2 ]Tianjin Agricultural University, Tianjin 300384, P.R. China
                [3 ]State Key Laboratory of Nutrition and Safety, Tianjin University of Science & Technology, Tianjin 300457, P.R. China
                [4 ]Phytomedicine and Pharmaceutical Biotechnology Excellence Center, Faculty of Pharmaceutical Sciences, Prince of Songkla University, Hat-Yai, Songkhla, 90112, Thailand
                Article
                10.1039/D1FO02324A
                34951619
                377b0f2d-9acc-413b-8c24-89ce51874c1b
                © 2022

                http://rsc.li/journals-terms-of-use

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