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Author(s): Francesco Asnicar [sup.1] , Sarah E. Berry [sup.2] , Ana M. Valdes [sup.3] [sup.4] , Long H. Nguyen [sup.5] , Gianmarco Piccinno [sup.1] , David A. Drew [sup.5] , [...], The gut microbiome is shaped by diet and influences host metabolism; however, these links are complex and can be unique to each individual. We performed deep metagenomic sequencing of 1,203 gut microbiomes from 1,098 individuals enrolled in the Personalised Responses to Dietary Composition Trial (PREDICT 1) study, whose detailed long-term diet information, as well as hundreds of fasting and same-meal postprandial cardiometabolic blood marker measurements were available. We found many significant associations between microbes and specific nutrients, foods, food groups and general dietary indices, which were driven especially by the presence and diversity of healthy and plant-based foods. Microbial biomarkers of obesity were reproducible across external publicly available cohorts and in agreement with circulating blood metabolites that are indicators of cardiovascular disease risk. While some microbes, such as Prevotella copri and Blastocystis spp., were indicators of favorable postprandial glucose metabolism, overall microbiome composition was predictive for a large panel of cardiometabolic blood markers including fasting and postprandial glycemic, lipemic and inflammatory indices. The panel of intestinal species associated with healthy dietary habits overlapped with those associated with favorable cardiometabolic and postprandial markers, indicating that our large-scale resource can potentially stratify the gut microbiome into generalizable health levels in individuals without clinically manifest disease. Analyses from the gut microbiome of over 1,000 individuals from the PREDICT 1 study, for which detailed long-term diet information as well as hundreds of fasting and same-meal postprandial cardiometabolic blood marker measurements are available, unveil new associations between specific gut microbes, dietary habits and cardiometabolic health.

Author(s): Suzie Ferrie [sup.1] [sup.2] , Amy Webster [sup.1] , Betty Wu [sup.3] , Charis Tan [sup.2] , Sharon Carey [sup.1] [sup.2] Author Affiliations: (1) University of Sydney, Sydney, Australia [...], Background/objectives The impact of gastrointestinal surgery on the profile of the human gut microbiome is not fully understood. This review aimed to identify whether there is a change to the profile of the gut microbiome as a result of gastrointestinal surgery. Subjects/methods In August 2018, a systematic literature search was conducted in Medline, PreMedline, Embase, CINAHL and The Cochrane Register of Clinical Trials, identifying and critically appraising studies which investigated changes to gut microbiome pre- and post-gastrointestinal surgery. Results Of 2512 results, 14 studies were included for analysis. All studies reported post-surgical change to the microbiome. In 9 of the 14 studies, prevalence of specific bacteria had significantly changed after surgery. Improved outcome was associated with higher levels of beneficial bacteria and greater microbiome diversity post-surgery. Conclusion There were methodological limitations in the included studies leading to uncertainty regarding the impact of gastrointestinal surgery alone on the microbiome profile. An ideal future model for research should encompass case-controlled or cohort design with longer term follow-up in a homogeneous patient group. Future research should seek to clarify the gold standard testing method and standardised timing for post-surgical microbiome sample collection. It is imperative that controls for confounders be put in place to attempt to identify the true association between gastrointestinal surgery and changes to gut microbiome.

Author(s): Bing Zhai [sup.1] , Mihaela Ola [sup.2] , Thierry Rolling [sup.1] [sup.3] , Nicholas L. Tosini [sup.1] , Sari Joshowitz [sup.1] , Eric R. Littmann [sup.4] , Luigi A. [...], The intestinal microbiota is a complex community of bacteria, archaea, viruses, protists and fungi.sup.1,2. Although the composition of bacterial constituents has been linked to immune homeostasis and infectious susceptibility.sup.3-7, the role of non-bacterial constituents and cross-kingdom microbial interactions in these processes is poorly understood.sup.2,8. Fungi represent a major cause of infectious morbidity and mortality in immunocompromised individuals, although the relationship of intestinal fungi (that is, the mycobiota) with fungal bloodstream infections remains undefined.sup.9. We integrated an optimized bioinformatics pipeline with high-resolution mycobiota sequencing and comparative genomic analyses of fecal and blood specimens from recipients of allogeneic hematopoietic cell transplant. Patients with Candida bloodstream infection experienced a prior marked intestinal expansion of pathogenic Candida species; this expansion consisted of a complex dynamic between multiple species and subspecies with a stochastic translocation pattern into the bloodstream. The intestinal expansion of pathogenic Candida spp. was associated with a substantial loss in bacterial burden and diversity, particularly in the anaerobes. Thus, simultaneous analysis of intestinal fungi and bacteria identifies dysbiosis states across kingdoms that may promote fungal translocation and facilitate invasive disease. These findings support microbiota-driven approaches to identify patients at risk of fungal bloodstream infections for pre-emptive therapeutic intervention. Expansion of pathogenic Candida species coupled with bacterial dysbiosis in the gut precedes Candida bloodstream infections in hematopoietic cell transplant recipients.

Digestive system functionality is a key process linked to larval recruitment and survival. However, little is known about organ development and enzyme maturation of the digestive system of North Sea Atlantic herring (Clupea harengus). In this study, herring larvae were reared at 13 °C from hatching to 69 day post hatch, covering four developmental stages: (1) yolk sac (8-9 mm), (2) pre-flexion (9-14 mm), (3) flexion (12-18 mm) and (4) post-flexion stages (15-30 mm). Combined histological (semi-quantitative scoring) and enzyme analyses (pancreatic and intestinal) showed that developmental stages are strongly linked to physiological changes. The larvae lack a functional stomach and use the intestine as the primary site of digestion which is mainly supported by pancreatic enzyme activity. The intestine acquired adult enzymatic digestive features with a functional brush border at the end of the flexion stage and pyloric ceca started to develop during the post-flexion stage. The transition from pre-flexion to flexion stage and the end of the post-flexion stage are energetically taxing periods as indicated by a reduced number and size of liver vacuoles. Based on these findings, we consider these moments as critical periods, where herring larvae could be dramatically affected by suboptimal feeding conditions in the field. This implies that pre-flexion stage larvae with low or no liver reserves may not be able to proceed to the next developmental stage. Hence, the level of energy storage in first-feeding larvae needs to be examined for its use as a field indicator of survival and development., Author(s): Léa J. Joly [sup.1] [sup.2] , Christophe Loots [sup.1] , Cédric L. Meunier [sup.2] , Maarten Boersma [sup.2] [sup.3] , Sophie Collet [sup.4] , Valérie Lefebvre [sup.1] , José-Luis [...]

Introduction Advanced cancers of the gastrointestinal (GI) tract are highly resistant to chemotherapy, radiotherapy, and biologicals (1). Even new immunotherapies benefit only a subset of patients with colorectal cancer (CRC) [...], The gastrointestinal tract comprises a complex ecosystem with extensive opportunities for functional interactions between neoplastic epithelial cells and stromal, immune, neuronal, glial, and other cell types, as well as microorganisms and metabolites within the gut lumen. In this Review, we focus on interactions between gastrointestinal cancers and elements of the central and enteric nervous systems. This previously understudied but rapidly emerging area of investigation has blossomed in recent years, particularly with respect to improved understanding of neural contributions to the development and progression of esophageal, gastric, pancreatic, and colon neoplasia. Cancer neuroscience offers great promise to advance our understanding of how neural-cancer interactions promote alimentary tract neoplasia. The resulting mechanistic insights can be leveraged to identify diagnostic and prognostic biomarkers, and to develop novel therapeutic interventions.

Introduction Given that the prevalence of obesity is approaching 50% in some countries (1), it is hard to argue that body weight/adiposity is regulated at healthy levels through biological mechanisms [...], Given the crucial role of the gastrointestinal tract and associated organs in handling nutrient assimilation and metabolism, it has long been known that its communication with the brain is important for the control of ingestive behavior and body weight regulation. It is also clear that gut-brain communication is bidirectional and utilizes both rapid neural and slower humoral mechanisms and pathways. However, progress in understanding these mechanisms and leveraging them for the treatment of obesity and metabolic disease has been hindered by the enormous dimension of the gut mucosa, the complexity of the signaling systems, and lack of specific tools. With the ascent of modern neurobiological technology, our understanding of the role of vagal afferents in gut-brain communication has begun to change. The first function-specific populations of vagal afferents providing nutritional feedback as well as feed-forward signals have been identified with genetics- guided methodology, and it is hoped that extension of the methodology to other neural communication pathways will follow soon. Currently, efficient clinical leveraging of gut-brain communication to treat obesity and metabolic disease is limited to a few gut hormones, but a more complete understanding of function-specific and projection-specific neuronal populations should make it possible to develop selective and more effective neuromodulation approaches.

Author(s): Danit Oz-Levi [sup.1] , Tsviya Olender [sup.1] , Ifat Bar-Joseph [sup.2] [sup.3] , Yiwen Zhu [sup.4] , Dina Marek-Yagel [sup.2] [sup.3] [sup.5] , Iros Barozzi [sup.4] [sup.23] , Marco [...], Large-scale genome sequencing is poised to provide a substantial increase in the rate of discovery of disease-associated mutations, but the functional interpretation of such mutations remains challenging. Here we show that deletions of a sequence on human chromosome 16 that we term the intestine-critical region (ICR) cause intractable congenital diarrhoea in infants.sup.1,2. Reporter assays in transgenic mice show that the ICR contains a regulatory sequence that activates transcription during the development of the gastrointestinal system. Targeted deletion of the ICR in mice caused symptoms that recapitulated the human condition. Transcriptome analysis revealed that an unannotated open reading frame (Percc1) flanks the regulatory sequence, and the expression of this gene was lost in the developing gut of mice that lacked the ICR. Percc1-knockout mice displayed phenotypes similar to those observed upon ICR deletion in mice and patients, whereas an ICR-driven Percc1 transgene was sufficient to rescue the phenotypes found in mice that lacked the ICR. Together, our results identify a gene that is critical for intestinal function and underscore the need for targeted in vivo studies to interpret the growing number of clinical genetic findings that do not affect known protein-coding genes. An intestine-critical region on human chromosome 16, and its regulation of PERCC1, a newly identified gene, is shown to underlie the genetic basis of a severe, inherited form of diarrhoea.

ABSTRACT Two hundred sixty-one octopuses were obtained from August 2006 to June 2007 in Bahia de Los Angeles, BC, Mexico. Sizes ranged from 58-190 mm in mantle length. Diet was [...]

INTRODUCTION Most wood decomposition in the digestive tract of subterranean termite workers (family Rhinotermitidae) occurs in food vacuoles of flagellate protozoan symbionts in the hindgut (Radek, 1999). Types of protozoa [...]

INTRODUCTION In the 1960s Altman and Das administered tritiated thymidine to adult rats to label dividing cells and demonstrated that neurogenesis occurs in the dentate gyrus and the olfactory bulb [...], It is unclear whether neurogenesis occurs in the adult mammalian enteric nervous system (ENS). Neural crest-derived cells capable of forming multilineage colonies in culture, and neurons and glia upon transplantation into chick embryos, persist throughout adult life in the mammalian ENS. In this study we sought to determine the physiological function of these cells. We discovered that these cells could be identified based on CD49b expression and that they had characteristics of enteric glia, including p75, GFAP, S100B, and SOX10 expression. To test whether new neurons or glia arise in the adult gut under physiological conditions, we marked dividing progenitors with a thymidine analog in rodents under steady-state conditions, or during aging, pregnancy, dietary changes, hyperglycemia, or exercise. We also tested gut injuries including inflammation, irradiation, benzalkonium chloride treatment, partial gut stenosis, and glial ablation. We readily observed neurogenesis in a neurogenic region of the central nervous system, but not reproducibly in the adult ENS. Lineage tracing of glial cells with GFAP-Cre and GFAP-CreERT2 also detected little or no adult ENS neurogenesis. Neurogenesis in the adult gut is therefore very limited under the conditions we studied. In contrast, ENS gliogenesis was readily observed under steady-state conditions and after injury. Adult enteric glia thus have the potential to form neurons and glia in culture but are fated to form mainly glia under physiological conditions and after the injuries we studied.

The interstitial cells of Cajal (ICC), as pacemaker cells of the gut, contribute to rhythmic peristalsis and muscle excitability through initiation of slow-wave activity, which subsequently actively propagates into the musculature. An E-4031-sensitive [K.sup.+] current makes a critical contribution to membrane potential in ICC. This study provides novel features of this current in ICC in physiological solutions and seeks to identify the channel isoform. In situ hybridization and Kit immunohistochemistry were combined to assess ether-a-go-go-related gene (ERG) mRNA expression in ICC in mouse jejunum, while the translated message was assessed by immunofluorescence colocalization of ERG and Kit proteins. E-4031-sensitive currents in cultured ICC were studied by the whole cell patch-clamp method, with physiological [K.sup.+] concentration in the bath and the pipette. In situ hybridization combined with Kit immunohistochemistry detected m-erg1 and m-erg3, but not m-erg2, mRNA in ICC. ERG3 protein was colocalized with Kit-immunoreactive ICC in jejunum sections, but ERG1 protein was visualized only in the smooth muscle cells. At physiological [K.sup.+] concentration, the E-4031-sensitive outward current in ICC was different from its counterpart in cardiac and gut smooth muscle cells. In particular, inactivation upon depolarization and recovery from inactivation by hyperpolarization were modest in ICC. In summary, the E-4031-sensitive currents influence the kinetics of the pacemaker activity in ICC and contribute to maintenance of the resting membrane potential in smooth muscle cells, which together constitute a marked effect on tissue excitability. Whereas this current is mediated by ERG1 in smooth muscle, it is primarily mediated by ERG3 in ICC. gastrointestinal motility; potassium channels; pacemaker activity

Serotonin or 5-hydroxytryptamine (5-HT) influences numerous functions in the gastrointestinal tract. We previously demonstrated that 5-HT treatment of Caco-2 cells inhibited [Na.sup.+]/[H.sup.+] exchangers (NHE) and [Cl.sup.-]/O[H.sup.-] exchange activities via distinct signaling mechanisms. Since regulation of several ion transporters such as NHE3 is influenced by intact cytoskeleton, we hypothesized that 5-HT modifies actin cytoskeleton and/or brush-border membrane architecture via involvement of signaling pathways. Ultrastructural analysis showed that 5-HT (0.1 [micro]M, 1 h) treatment of Caco-2 cells caused the apical membrane to assume a convex dome shape that was associated with shortening of microvilli. To examine whether these cellular architecture changes are cytoskeleton driven, we analyzed actin cytoskeleton by fluorescence microscopy. 5-HT induced basal stress fibers with prominent cortical actin filaments via 5-HT3 and 5-HT4 receptor subtypes. This induction was partially attenuated by chelation of intracellular [Ca.sup.2+] and PKC[alpha] inhibition (Go6976). In vitro assays revealed that PKC[alpha] interacted with actin and this association was increased by 5-HT. Our data provide novel evidence that 5-HT-induced signaling via 5-HT3/4 receptor subtypes to cause [Ca.sup.2+] and PKC[alpha]-dependent regulation of actin cytoskeleton may play an important role in modulation of ion transporters that contribute to pathophysiology of diarrheal conditions associated with elevated levels of 5-HT. microvilli; serotonin and actin; 5-HT and curvature; stress fibers; ion transporter; cytoskeleton

Abstract: We investigated the digestive potential of the stream detritivore Tipula lateralis Meigen, 1804 as a tool to understand and predict their ability to adapt to environmental changes, such as [...]

'Tell me what you eat, and I will tell you what you are,' wrote the French gastronome Jean Brillat-Savarin in 1826 (1). Although at the time of Brillat-Savarin the connection [...], The enteric nervous system has been studied thus far as an isolated unit. As researchers probe deeper into the function of this system, it is evident that the neural network stretches beyond enteric neurons. It is formed by both intrinsic and extrinsic neurons innervating the gut, enteric glia, and innervated sensory epithelial cells, such as enteroendocrine cells. This Review series summarizes recent knowledge on function and disease of nerves, glia, and sensory epithelial cells of the gut in eight distinctive articles. The timing and growing knowledge for each individual field calls for an appropriate term encompassing the entire system. We call this neuronal ensemble the 'gut connectome' and summarize the work from a food sensory perspective.

The digestive glands of four groups of mussels (Mytilus galloprovincialis) were examined under light and electron microscopes. Individuals of the first group were fixed immediately after their extraction from seawater; those of the second, after having been kept out of water for 2 h; while those of the third and fourth groups, after maintenance in the aquarium for 1 day and 1 week, respectively. The digestive gland cells of the mussels kept out of the water for 2 h presented, in many cases, extensive morphological disorganization, expressed mainly by cytoplasmic extrusions into the tubule lumen. In contrast, the mussels kept in the aquarium for 1 day showed no disintegration phenomena in their digestive cells, but presented a decrease in the height of the tubule epithelium and increased size of the tubule lumen. Similarly, the mussels kept in the aquarium for 1 week presented cells characterized by increased height compared to those of the mussels of the previous group, as well as a quite inactive epithelium, with no extrusion of cytoplasmic materials into the lumen. The values of the 'lysosomal membrane stability' test (LMS), a bioindicator of general stress, were also evaluated. The mussels kept in the aquarium for 1 day showed decreased LMS values compared to the values for other mussel groups, which indicated that general stress had increased. Results of the present study show that care should be taken in sampling and handling of mussels for use in biomonitoring studies.

The binding of Steel factor (SF) to c-kit initiates a signaling pathway essential for development and maintenance of interstitial cells of Cajal (ICC). Soluble and membrane-bound isoforms of SF are expressed in the gastrointestinal tract, but the role for either isoform in supporting ICC development is unknown. The aim of this study was to determine the role of SF in supporting ICC in culture. ICC were cultured from dissociated mouse jejunum and grown with fibroblast cell lines that produced either soluble, membrane-bound or membrane-restricted SF. ICC were identified and counted by c-kit immunoreactivity. The number of c-kit immunoreactive cells was greater in the coculture system compared with cultures grown without SF-producing fibroblasts. All forms of SF-producing fibroblasts increased ICC number in culture but physical separation of the fibroblasts from the c-kit immunoreactive cells, the addition of exogenous SF to the culture medium, or fibroblast-conditioned media did not. These results are consistent with the hypothesis that the membranebound form of SF preferentially contributes to expression of c-kit-positive ICC under cell culture conditions. immunocytochemistry; gastrointestinal pacemaker; Steelfactor proteolysis

Despite the essential functions of the digestive system, much remains to be learned about the cellular and molecular mechanisms responsible for digestive organ morphogenesis and patterning. We introduce a novel zebrafish transgenic line, the gutGFP line, that expresses GFP throughout the digestive system, and use this tool to analyze the development of the liver. Our studies reveal two phases of liver morphogenesis: budding and growth. The budding period, which can be further subdivided into three stages, starts when hepatocytes first aggregate, shortly after 24 h postfertilization (hpf), and ends with the formation of a hepatic duct at 50 hpf. The growth phase immediately follows and is responsible for a dramatic alteration of liver size and shape. We also analyze gene expression in the developing liver and find a correlation between the expression of certain transcription factor genes and the morphologically defined stages of liver budding. To further expand our understanding of budding morphogenesis, we use loss-of-function analyses to investigate factors potentially involved in this process. It had been reported that no tail mutant embryos appear to lack a liver primordium, as assessed by gata6 expression. However, analysis of gutGFP embryos lacking Ntl show that the liver is in fact present. We also find that, in these embryos, the direction of liver budding does not correlate with the direction of intestinal looping, indicating that the left/right behavior of these tissues can be uncoupled. In addition, we use the cloche mutation to analyze the role of endothelial cells in liver morphogenesis, and find that in zebrafish, unlike what has been reported in mouse, endothelial cells do not appear to be necessary for the budding of this organ. Keywords: Endoderm; Hepatocytes; Chirality; cloche

The digestive gland of the marine mussel Mytilus edulis has been studied using primary cell culture of digestive-gland cells in a time-course study of antioxidant- and biotransformation-enzyme activity and ultrastructural changes. Invertebrate toxicological studies were of interest. A pattern of change seen in activity levels may be related to differential cell survival. Activities of biotransformation enzymes decrease faster over time than activities of two antioxidation enzymes. It may be that antioxidant enzyme activity is more stable vs time than the activity of biotransformation enzymes. Capacity of xenobiotic metabolism may be mainly in large digestive cells. Primary cell cultures from invertebrate species may give useful tools for characterization studies for viruses and pathogens.

This study was designed to determine the nutritional lipid requirement of seabass larvae and to understand the effects of dietary fat concentration on their digestive tract maturation. Seabass (Dicentrarchus labrax) larvae were fed, from d 15 to 38 of life, one of five isonitrogenous compound diets with different lipid levels, ranging from 10 to 30 g/100 g. The higher the lipid level, the greater the growth and survival of the larvae (P < 0.05). The lipolytic enzymes assayed, lipase and phospholipase [A.sub.2], were stimulated by the increase in their respective dietary substrates, triglycerides and phospholipids, in 38-d-old larvae (P < 0.05). Nevertheless, a plateau in the activity of these two lipolytic enzymes was observed from 20% dietary lipids onwards. The similar mRNA levels of phospholipase [A.sub.2] in the three groups fed the highest lipid levels suggested that the maximal synthesis level of lipolytic enzyme was reached at 20% dietary fat. Pancreatic secretion of trypsin and amylase were positively affected by the dietary lipid level; a possible involvement of a cholecystokinin-releasing factor is discussed. Diets containing >20% lipids led to the increase in activities of brush border membrane enzymes to the detriment of a cytosolic enzyme in enterocytes, leucine-alanine (Leu-Ala) peptidase. This enzymatic change reveals the earlier maturation of enterocytes in larva groups fed high lipid levels. KEY WORDS: Dicentrarchus labrax; dietary lipid; pancreatic enzymes; intestinal enzymes

Certain mechanisms govern the adhesion of leukocytes to vascular endothelial cells in the digestive system. The presence of circulating soluble isoforms of endothelial cell adhesion molecules (CAMs), for instance, suggest their potential as endogenous anti-inflammatory agents. Also, upstream components of the microcirculation can play a role in the sequestration of circulating leukocytes within inflamed tissue. These upstream vascular segments may be responsive to adhesion-dependent leukocyte-endothelial cell interactions that exist within postcapillary venules.

The interplay between suckling, intestinal growth and brush-border membrane functions is critical during the perinatal period. The present study investigates changes in intestinal dimensions, activities of four brush border membrane hydrolases (lactase, sucrase, maltase and aminooligopeptidase) and rates of sugar and amino acid uptake by intact tissues and brush border membrane vesicles during the first 24 h of suckling. Total intestinal weight, mucosal weight and protein content increased 58%, 80% and 126% (P < 0.05) during the first 6 h of suckling; length and surface area did not increase. Total mucosal DNA content was 4.6-fold higher at 24 h after birth, with the rate of increase differing among intestinal regions. Hydrolytic capacities of the entire small intestine increased, more so for homogenates than for brush border membrane vesicles, and more for lactase relative to the other hydrolases studied. Rates of nutrient transport declined, especially for brush border membrane vesicles, for proximal and mid-intestine relative to distal intestine, and for glucose relative to galactose and amino acids. We conclude that 1) changes in brush border membrane digestive functions coincide with rapid intestinal growth, with postnatal patterns varying among hydrolases, transporters and regions; 2) insertion into the brush border membrane, not synthesis, limits the postnatal increase of hydrolase activity; and 3) despite declines in specific activity, hydrolytic and glucose transport capacities of the entire intestine remained stable or increased, and exceeded estimated dietary loads because of intestinal growth. KEY WORDS: * colostrum * neonatal * pigs * nutrient transport * brush border hydrolases

The Caenorhabditis elegans digestive tract is composed of four distinct modules derived from separate cell lineages: anterior pharynx from the ABa lineage, posterior pharynx from the MS lineage, gut from the E lineage, and rectum from the ABp lineage. The C. elegans gut esterase gene (ges-1) is normally expressed in the embryonic gut or E lineage. However, expression of ges-1 can be switched into cells of the embryonic pharynx and tail by virtue of deleting a tandem pair of WGATAR sites in the ges-1 promoter. Here, we use both laser ablation experiments and genetic analysis to show that cells expressing the WGATAR-deleted ges-1 transgene belong to all three nongut lineages of the digestive tract: ABa, MS, and ABp. We also show that the molecular size and spatial distribution of ges-1 mRNA transcripts produced by either the WGATAR-deleted ges-1 transgene or the undeleted ges-1 control transgene appear correctly regulated, suggesting that the spatial switch in ges-1 expression occurs at the level of transcription initiation. We further show that both the WGATAR-deleted and the undeleted ges-1 transgenes respond appropriately to mutations in a series of maternal effect genes (skn-1, mex-1, pie-1, and pop-1) that alter early blastomere fate. Moreover, the pharynx/tail expression of the WGATAR-deleted ges-1 transgene is abolished by mutations in the zygotic gene pha-4. Finally, we use imprecise transposon excision to produce two independent C. elegans strains with 1- to 2-kb deletions that remove the tandem WGATAR sites from the promoter of the endogenous chromosomal ges-1 gene: in both of these strains, ges-1 is not expressed in the embryonic gut but is expressed in cells of the embryonic pharynx; pharynx expression is weak but incontrovertible. Overall, our results validate previous transgenic analysis of ges-1 control and show further that ges-1 appears to be regulated in a system-specific, rather than a lineage-specific, manner. The multiple facets of ges-1 expression provide an opportunity to investigate how a multicomponent organ system such as the digestive tract is established from diverse cell lineages.

Male Canvasbacks' failure to show deficits in nutrient reserves of somatic lipids, proteins and minerals, may be attributable to the nutritional requirements for molt. Ingesta-free body mass of male Canvasbacks is minimum during remigial molt, and fluctuates with storage and catabolism of lipids. The birds have low reliance on endogenous fat, protein and mineral to satisfy nutrient requirements for molt. The total body protein during postreproductive molts remains quite stable, but shows alterations in the distribution of muscle tissue in molting birds.

Introduction The digestive gland (also known as the midgut gland or hepatopancreas) of decapod crustaceans serves the dual role of secreting enzymes and absorbing digested food. This gland is composed [...], We determined the role of the digestive gland in the respiratory metabolism of Penaeus setiferus adult males as a step toward proposing a feeding schedule based on the cycle of activity the digestive gland. We measured pre- and postprandial values for oxygen consumption rate and hemolymph glucose concentrations in live animals, and oxygen consumption rate and glycogen concentration in excised digestive gland. After the animals were fed, which enhanced general metabolic activity, these indices changed. There was a high correlation between the oxygen consumption rate of the animal and the glucose concentration in the hemolymph, and between the oxygen consumption rate by the digestive gland and the glycogen concentration in the digestive gland, all in relation to time after feeding. Correlations support the hypothesis that the energy demand depends upon the metabolic substrate concentration. In this theory, glucose sustains muscle activity (during ingestion of food) and glycogen is the product of the digestive gland during food assimilation. Our observations of metabolic dynamics during the feeding period allowed us to examine the feeding process. The metabolic activity of the digestive gland was highest 6 h after feeding. This could mean that assimilation, having started 2 h after food intake, peaked 6 h after feeding. Eight hours after feeding, the oxygen consumption rate of the digestive gland decreased and fell to values similar to those recorded for animals subjected to 72 h of fasting.