Microalgae are a renewable and sustainable source of bioactive compounds, such as essential amino acids, polyunsaturated fatty acids, and antioxidant compounds, that have been documented to have beneficial effects on nutrition and health. Among these natural products, the demand for natural antioxidants, as an alternative to synthetic antioxidants, has increased. The antioxidant activity of microalgae significantly varies between species and depends on growth conditions. In the last decade, microalgae have been explored in livestock animals as feed additives with the aim of improving both animals’ health and performance as well as product quality and the environmental impact of livestock. These findings are highly dependent on the composition of microalgae strain and their amount in the diet. The use of carbohydrate-active enzymes can increase nutrient bioavailability as a consequence of recalcitrant microalgae cell wall degradation, making it a promising strategy for monogastric nutrition for improving livestock productivity. The use of microalgae as an alternative to conventional feedstuffs is becoming increasingly important due to food–feed competition, land degradation, water deprivation, and climate change. However, the cost-effective production and use of microalgae is a major challenge in the near future, and their cultivation technology should be improved by reducing production costs, thus increasing profitability.

Microalgae as a Sustainable Source of Antioxidants in Animal Nutrition, Health and Livestock Development

Butter has become renowned among consumers because of its exceptional flavor and taste. Nevertheless, conventional butter is deemed “unhealthy” due to its high concentration of saturated fats and cholesterol, which are linked to the development of cardiovascular ailments. Improving the health benefits of butter has become an essential topic of research in the butter industry. This review focuses on researches that have made improvements to functionality of butter, including the changes in fatty acid composition, cholesterol reduction, incorporation with bioactive substances, development of new sources. The reduction of saturated fatty acids and cholesterol in butter can help reduce the risk of disease from eating butter. In addition, incorporating probiotics or natural plant extracts can achieve nutritional functions such as balancing intestinal flora, enhancing nutrient absorption, and increasing the body's antioxidant capacity. Butter substitute products can be based on new vegetable oils, insect fats or microbial fats, which cater to the consumer demands for low-calorie butter while reducing the environmental impact that results from butter production. This review summarizes the effects and characteristics of various improvement methods and proposes some possible directions for future development of functional butter. 

Functional butter for reduction of consumption risk and improvement of nutrition

Liver-specific actions of GH and IGF1 that protect against MASLD.

Growth hormone attenuates obesity and reshapes gut microbiota in high-fat diet-fed mice

Patients with post-cholecystectomy (PC) often experience adverse gastrointestinal conditions, such as PC syndrome, colorectal cancer (CRC), and non-alcoholic fatty liver disease (NAFLD), that accumulate over time. An epidemiological survey further revealed that the risk of cholecystectomy is associated with high-fat and high-cholesterol (HFHC) dietary intake. Mounting evidence suggests that cholecystectomy is associated with disrupted gut microbial homeostasis and dysregulated bile acids (BAs) metabolism. However, the effect of an HFHC diet on gastrointestinal complications after cholecystectomy has not been elucidated. Here, we aimed to investigate the effect of an HFHC diet after cholecystectomy on the gut microbiota-BA metabolic axis and elucidate the association between this alteration and the development of intestinal inflammation. In this study, a mice cholecystectomy model was established, and the levels of IL-Iβ, TNF-α, and IL-6 in the colon were increased in mice fed an HFHC diet for 6 weeks. Analysis of fecal BA metabolism showed that an HFHC diet after cholecystectomy altered the rhythm of the BA metabolism by upregulating liver CPY7A1, CYP8B1, and BSEP and ileal ASBT mRNA expression levels, resulting in increased fecal BA levels. In addition, feeding an HFHC diet after cholecystectomy caused a significant dysbiosis of the gut microbiota, which was characterized by the enrichment of the metabolic microbiota involved in BAs; the abundance of pro-inflammatory gut microbiota and related pro-inflammatory metabolite levels was also significantly higher. In contrast, the abundance of major short-chain fatty acid (SCFA)-producing bacteria significantly decreased. Overall, our study suggests that an HFHC diet after cholecystectomy promotes intestinal inflammation by exacerbating the gut microbiome and BA metabolism dysbiosis in cholecystectomy. Our study also provides useful insights into the maintenance of intestinal health after cholecystectomy through dietary or probiotic intervention strategies.

A High-Fat, High-Cholesterol Diet Promotes Intestinal Inflammation by Exacerbating Gut Microbiome Dysbiosis and Bile Acid Disorders in Cholecystectomy.

Omega-3 PUFAs rich in fish oil are believed to prevent obesity by improving lipid metabolism and regulating gut microbiota. Microalgae oil is considered as an alternative source of omega-3 PUFAs owing to diminishing fish resources. Schizochytrium microalgae oil (SMO), with a high DHA proportion, is a promising source for commercial DHA production. However, its weight-loss and gut microbiota-regulating properties are not well studied. Here we compared the obesity reducing effects of SMO, commercial fish oil (FO) and a weight-loss drug, Orlistat (OL), in a high-fat diet (HFD) induced obesity mouse model. We found that SMO is comparable to commercial FO and OL with regard to weight loss, and it even exhibits the weight-loss effects earlier than FO and OL. It can efficiently inhibit the expression of lipogenesis-related genes and induce the expression of lipolysis-related genes. Moreover, SMO has different gut microbiota modulating effects from those of FO and OL. It does not influence the diversity of bacterial community, but does increase the abundance of several beneficial SCFAs-producing bacteria and inhibits obesity-promoting Desulfovibrio and several pathogens. We also found that SMO recovers the HFD-disturbed metabolic capability of gut microbiota. It can increase the abundance of several metabolism-related pathways, such as those of amino acids, SCFAs and bile acid, and decrease the level of the LPS biosynthesis pathway, which probably contributes to an improvement of lipid metabolism and restoration of the colonic mucosal barrier impaired by HFD. Our data suggest that SMO can be used as a superior dietary supplement for alleviating obesity.

Microalgae oil from Schizochytrium sp. alleviates obesity and modulates gut microbiota in high-fat diet-fed mice.

ABSTRACT Both growth hormone (GH) and gut microbiota play significant roles in diverse physiological processes, but the crosstalk between them is poorly understood. Despite the regulation of GH by gut microbiota, study on GH’s influence on gut microbiota is limited, especially on the impacts of tissue specific GH signaling and their feedback effects on the host. In this study, we profiled gut microbiota and metabolome in tissue-specific GHR knockout mice in the liver (LKO) and adipose tissue (AKO). We found that GHR disruption in the liver rather than adipose tissue affected gut microbiota. It changed the abundance of Bacteroidota and Firmicutes at phylum level as well as abundance of several genera, such as Lactobacillus, Muribaculaceae, and Parasutterella, without affecting α-diversity. Moreover, the impaired liver bile acid (BA) profile in LKO mice was strongly associated with the change of gut microbiota. The BA pools and 12-OH BAs/non-12-OH BAs ratio were increased in the LKO mice, which was due to the induction of CYP8B1 by hepatic Ghr knockout. Consequently, the impaired BA pool in cecal content interacted with gut bacteria, which in turn increased the production of bacteria derived acetic acid, propionic acid, and phenylacetic acid that were possible to participate in the impaired metabolic phenotype of the LKO mice. Collectively, our findings suggested that the liver GH signaling regulates BA metabolism by its direct regulation on CYP8B1, which is an important factor influencing gut microbiota. Our study is significant in exploring gut microbiota modification effects of tissue-specific GH signaling as well as its involvement in gut microbiota–host interaction.

https://www.tandfonline.com/doi/pdf/10.1080/19490976.2023.2221098?needAccess=true&role=button

Deletion of hepatic growth hormone receptor (GHR) alters the mouse gut microbiota by affecting bile acid metabolism

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Microalgae oil from Schizochytrium sp. alleviates obesity and modulates gut microbiota in high-fat diet-fed mice.

Deletion of hepatic growth hormone receptor (GHR) alters the mouse gut microbiota by affecting bile acid metabolism