Impact of Gut Microbiota on Host Glycemic Control DOI Creative Commons

Céline Gérard,

Hubert Vidal

Frontiers in Endocrinology, Год журнала: 2019, Номер 10

Опубликована: Янв. 29, 2019

Given that obesity and associated disorder type II diabetes mellitus have reached epidemic proportions worldwide, the development of efficient prevention therapeutic interventions is a global public health interest. There now large body evidence suggesting micro-organisms colonizing human gut, known as gut microbiota, play central role in physiology metabolism. Understanding how microbiota affects regulates key metabolic functions such glucose regulation insulin resistance an important issue. The present review summarizes recent advances our understanding bacterial species interfere with host phenotype. We will examine biological molecular mechanisms underlying impact on glycemic control including: incretin secretion, short-chain fatty acid production, bile metabolism adipose tissue regulation. highlight prebiotic/probiotic affect these processes are considered promising approaches to treat obese diabetic patients.

Язык: Английский

Microbiome—Microbial Metabolome—Cancer Cell Interactions in Breast Cancer—Familiar, but Unexplored DOI Creative Commons
Edit Mikó, Tündé Kovàcs,

Éva Sebő

и другие.

Cells, Год журнала: 2019, Номер 8(4), С. 293 - 293

Опубликована: Март 29, 2019

Breast cancer is a leading cause of death among women worldwide. Dysbiosis, an aberrant composition the microbiome, characterizes breast cancer. In this review we discuss changes to metabolism cells, as well and gut microbiome in The role unresolved, nevertheless it seems that does have pathology disease. secretes bioactive metabolites (reactivated estrogens, short chain fatty acids, amino acid metabolites, or secondary bile acids) modulate We highlight bacterial species taxonomical units generate these show their mode action, how affect mitochondrial other molecular events These resemble human hormones, they are produced "gland" (in case, microbiome) subsequently transferred distant sites action through circulation. appear be important constituents tumor microenvironment. Finally, dysbiosis interferes with treatment interfering chemotherapeutic drug availability.

Язык: Английский

Процитировано

183

Gut Microbiota Dysbiosis Drives and Implies Novel Therapeutic Strategies for Diabetes Mellitus and Related Metabolic Diseases DOI Creative Commons
Xuan Li,

Keita Watanabe,

Ikuo Kimura

и другие.

Frontiers in Immunology, Год журнала: 2017, Номер 8

Опубликована: Дек. 20, 2017

Accumulating evidence over the past decade has linked development of metabolic syndrome related to diabetes variations in gut microbiota, an emerging, critical homeostatic regulator host energy metabolism and immune responses. Mechanistic studies rodent models have revealed ever-increasing multitude molecular mechanisms whereby microbiota interacts with a variety sensing signaling pathways, leading modulation endocrine system, responses, nervous system activity, hence, predisposition diseases. Remarkably, microbiota-driven responses tissues nutrient-sensing microbial metabolites, particular short-chain fatty acids (SCFAs), been significantly associated proneness disorders. This review will synthesize recent efforts on unraveling mediating role pathogenesis diseases, aiming reveal new therapeutic opportunities.

Язык: Английский

Процитировано

182

Balancing Herbal Medicine and Functional Food for Prevention and Treatment of Cardiometabolic Diseases through Modulating Gut Microbiota DOI Creative Commons
Ming Lyu, Yuefei Wang,

Guanwei Fan

и другие.

Frontiers in Microbiology, Год журнала: 2017, Номер 8

Опубликована: Ноя. 8, 2017

It has become apparent that gut microbiota is closely associated with cardiometabolic diseases (CMDs), and alteration in microbiome compositions also linked to the host environment. Next generation sequencing (NGS) facilitated in-depth studies on effects of herbal medicine functional food microbiota. Both contain fiber, polyphenols polysaccharides, exerting prebiotics-like activities prevention treatment CMDs. The administrations lead increased abundance phylum Bacteroidetes, genus Akkermansia, Bifidobacteria, Lactobacillus, Bacteroides Prevotella, while reducing Firmicutes Firmicutes/Bacteroidetes ratio gut. interact alter microbial metabolites including short-chain fatty acids (SCFAs), bile (BAs) lipopolysaccharides (LPS), which are now correlated metabolic such as type 2 diabetes (T2D), obesity non-alcoholic liver disease (NAFLD). In addition, trimethylamine (TMA)-N-oxide (TMAO) recently atherosclerosis (AS) cardiovascular (CVD) risks. Moreover, gut-organs axes may serve potential strategy for treating CMDs intervention food. summary, a balance between rich polysaccharides plays vital role modulating (phylum ratio, Prevotella) through SCFAs, BAs, LPS TMAO signaling regarding Targeting new therapeutic by future. This review aims summarize utilized

Язык: Английский

Процитировано

179

Sodium butyrate reduces high-fat diet-induced non-alcoholic steatohepatitis through upregulation of hepatic GLP-1R expression DOI Creative Commons

Da Zhou,

Yuanwen Chen, Zehua Zhao

и другие.

Experimental & Molecular Medicine, Год журнала: 2018, Номер 50(12), С. 1 - 12

Опубликована: Дек. 1, 2018

Glucagon-like peptide-1 (GLP-1) has a broad spectrum of biological activity by regulating metabolic processes via both the direct activation class B family G protein-coupled receptors and indirect nonreceptor-mediated pathways. GLP-1 receptor (GLP-1R) agonists have significant therapeutic effects on non-alcoholic fatty liver disease (NAFLD) steatohepatitis (NASH) in animal models. However, clinical studies indicated that treatment had little effect hepatic steatosis some NAFLD patients, suggesting resistance may occur these patients. It is well-known gut metabolite sodium butyrate (NaB) could promote secretion from intestinal L cells. it unclear whether NaB improves responsiveness NAFLD. In current study, we showed serum levels patients were similar to those normal controls, but GLP-1R expression was significantly downregulated Similarly, mouse model, mice fed with high-fat diet reduced expression, which reversed accompanied markedly alleviated steatosis. addition, also upregulated p-AMPK/p-ACC insulin receptor/insulin substrate-1 levels. Furthermore, NaB-enhanced HepG2 cells inhibiting histone deacetylase-2 independent GPR43/GPR109a. These results indicate able prevent progression NAFL NASH promoting expression. sensitizer represents potential adjuvant NASH. A for incorporates found more serious condition. Drugs enhance glucagon-like (GLP-1), protein involved processes, shown promise targeting condition, steatohepatitis. appear resistant treatment. Jian-Gao Fan at Shanghai Jiao Tong University China, Huiping Zhou McGuire VA Medical Center Richmond, USA, co-workers demonstrated called help encourage The team considerably compared healthy controls. Experiments models incorporating improved deposits.

Язык: Английский

Процитировано

177

Impact of Gut Microbiota on Host Glycemic Control DOI Creative Commons

Céline Gérard,

Hubert Vidal

Frontiers in Endocrinology, Год журнала: 2019, Номер 10

Опубликована: Янв. 29, 2019

Given that obesity and associated disorder type II diabetes mellitus have reached epidemic proportions worldwide, the development of efficient prevention therapeutic interventions is a global public health interest. There now large body evidence suggesting micro-organisms colonizing human gut, known as gut microbiota, play central role in physiology metabolism. Understanding how microbiota affects regulates key metabolic functions such glucose regulation insulin resistance an important issue. The present review summarizes recent advances our understanding bacterial species interfere with host phenotype. We will examine biological molecular mechanisms underlying impact on glycemic control including: incretin secretion, short-chain fatty acid production, bile metabolism adipose tissue regulation. highlight prebiotic/probiotic affect these processes are considered promising approaches to treat obese diabetic patients.

Язык: Английский

Процитировано

177