Microbiota-derived lactate accelerates colon epithelial cell turnover in starvation-refed mice

Okada, Toshihiko; Fukuda, Shinji; Hase, Koji; Nishiumi, Shin; Izumi, Yuichi; Yoshida, Masaru; Hagiwara, Tokio; Kawashima, Rei; Yamazaki, Motomi; Oshio, Tomoyuki; Otsubo, Takeshi; Inagaki–Ohara, Kyoko; Kakimoto, Kazuki; Higuchi, Kazuhide; Kawamura, Yuki I.; Ohno, Hiroshi; Dohi, Taeko

doi:10.1038/ncomms2668

Cited by 123 publications

(109 citation statements)

References 39 publications

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“…The lactic acid produced might help lower the pH and inhibit amino acid degradation in the colon 24,39 . Lactobacillus and Bifidobacterium have been found to stimulate NADPH oxidase 1-dependent ROS generation and intestinal stem cell proliferation 47 , and lactate was reported to accelerate colon epithelial cell turnover in starvation-refed mice 48 . Thus, advanced colorectal adenoma or carcinoma patients appear to be deficient in lactic acid-producing commensals such as Bifidobacterium that could promote daily renewal of the colon epithelium and inhibit potential pathogens.…”

Section: Discussionmentioning

confidence: 99%

Gut microbiome development along the colorectal adenoma–carcinoma sequence

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Gut microbiome development along the colorectal adenoma–carcinoma sequence

et al. 2015

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“…For rats, colonic cell proliferation decreases during a 36-h fast and rapidly resumes upon refeeding (416). Within 6 h of refeeding, cell proliferation rates had returned to control (fed) values, after which rates continued to increase to peak at 24 h, before returning to control levels after 76 h of refeeding (416).…”

Section: Large Intestine and Cecummentioning

confidence: 97%

“…The absence of enteral nutrients leads to atrophy of the small intestinal mucosa (i.e., villi, crypts, and lamina propria). This is due in part to the fasting-induced reduction in local (epithelial) and neuroendocrine signals that promote epithelial cell function and proliferation (294), and to the reduction in luminal molecules, including those from dietary and microbial sources that can stimulate mucosal growth (416). Depending on species, fasting for as little as 24 h can cause intestinal atrophy, due primarily to shortening of villi and, to a lesser extent, crypts, with a coordinate reduction in total mucosal mass ( Fig.…”

Section: Small Intestinementioning

confidence: 99%

Integrative Physiology of Fasting

Secor

Carey

2016

Comprehensive Physiology

132

144

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Extended bouts of fasting are ingrained in the ecology of many organisms, characterizing aspects of reproduction, development, hibernation, estivation, migration, and infrequent feeding habits. The challenge of long fasting episodes is the need to maintain physiological homeostasis while relying solely on endogenous resources. To meet that challenge, animals utilize an integrated repertoire of behavioral, physiological, and biochemical responses that reduce metabolic rates, maintain tissue structure and function, and thus enhance survival. We have synthesized in this review the integrative physiological, morphological, and biochemical responses, and their stages, that characterize natural fasting bouts. Underlying the capacity to survive extended fasts are behaviors and mechanisms that reduce metabolic expenditure and shift the dependency to lipid utilization. Hormonal regulation and immune capacity are altered by fasting; hormones that trigger digestion, elevate metabolism, and support immune performance become depressed, whereas hormones that enhance the utilization of endogenous substrates are elevated. The negative energy budget that accompanies fasting leads to the loss of body mass as fat stores are depleted and tissues undergo atrophy (i.e., loss of mass). Absolute rates of body mass loss scale allometrically among vertebrates. Tissues and organs vary in the degree of atrophy and downregulation of function, depending on the degree to which they are used during the fast. Fasting affects the population dynamics and activities of the gut microbiota, an interplay that impacts the host's fasting biology. Fasting-induced gene expression programs underlie the broad spectrum of integrated physiological mechanisms responsible for an animal's ability to survive long episodes of natural fasting.

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“…Measurement of thymidine or Brdu incorporation has shown that the circadian rhythm mediates the proliferation of the intestinal epithelium in both humans and rodents (90 -93). This rhythm persisted under fasting in mice (94), and expression was dramatically enhanced by re-feeding (93).…”

Section: Intestinal Epitheliummentioning

confidence: 89%

Chrono-biology, Chrono-pharmacology, and Chrono-nutrition

Tahara¹,

Shibata²

2014

J Pharmacol Sci

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Molecular mechanisms of the circadian clock systemThe circadian clock system has been widely maintained in many species, from prokaryotes to mammals. "Circadian" means "around [a] day" in Latin, and therefore "circadian rhythm" refers to a cycle of approximate 24 h. The earth rotates once every 24 h, and the circadian system has evolved to adjust functions and behavior to this cycle in order to efficiently utilize sunlight for photosynthesis in the case of plants and cyanobacteria and to obtain food in the case of animals. One of the most important features of our circadian system is that circadian clocks can endogenously maintain time under constant darkness and without external stimuli, suggesting that our body has its own internal clocks. In 1972, Moore and Eichler (1) investigated the effects of destroying the suprachiasmatic nucleus (SCN) in the rat hypothalamus. Their results revealed the loss of sleep-wake cycles and corticosterone rhythms. Since then, the SCN is regarded as the location of the master clock system in mammals. The SCN receives light-dark information directly through the retinal-hypothalamic tract and organizes the local clock in the peripheral tissues through multiple pathways involving neural and hormonal functions (2, 3). The molecular mechanism of the circadian system in mammals has been well studied over the past two decades. The transcriptional-translational feedback loop of the major clock genes Bmal1, Clock, Per1/2, and Cry1/2 is the main component of the circadian system (2) (Fig. 1A). Bmal1 and Clock, which are transcriptional activators, play a positive role in activating the Per and Cry genes through a specific promoter sequence known as the E-box. Per and Cry are translated into proteins in the cytoplasm and are then transported back into the nucleus after interacting with each other, and they subsequently stop their transcription by binding to BMAL1 and CLOCK. Thus, Per and Cry are rhythmically expressed over a 24-h period. This transcriptional regulation induces rhythmic expression of approximately 10% of all genes in each peripheral cell (4 -6). In addition to such transcriptional regulation of the circadian clock, post-transcriptional regulation and translational regulation have recently been reported to play important roles in maintaining circadian rhythms. Genome-wide RNA-seq and Chip-seq analyses found that only 22% of the rhythmically oscillating messenger RNAs are driven by de novo transcription, with RNA polymerase II recruitment and chromatin remodeling also exhibiting such rhythms (7). Furthermore, it was reported that the non-transcriptional redox cycle has a 24-h rhythm in Chrono-biology, Chrono-pharmacology, and Chrono-nutrition Tokyo 162-8480, Japan Received October 25, 2013; Accepted January 5, 2014 Abstract. The circadian clock system in mammals drives many physiological processes including the daily rhythms of sleep-wake behavior, hormonal secretion, and metabolism. This system responds to daily environmental changes, such as the light-dark cycle, food...

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Microbiota-derived lactate accelerates colon epithelial cell turnover in starvation-refed mice

Cited by 123 publications

References 39 publications

Gut microbiome development along the colorectal adenoma–carcinoma sequence

Gut microbiome development along the colorectal adenoma–carcinoma sequence

Integrative Physiology of Fasting

Chrono-biology, Chrono-pharmacology, and Chrono-nutrition

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