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The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the gut-derived hormones affecting metabolic and behavioral responses are poorly defined. Here we show that the endocrine cells of the Drosophila gut sense nutrient stress through a mechanism that involves the TOR pathway and in response secrete the peptide hormone allatostatin C, a Drosophila somatostatin homolog. Gut-derived allatostatin C induces secretion of glucagon-like adipokinetic hormone to coordinate food intake and energy mobilization. Loss of gut Allatostatin C or its receptor in the adipokinetic-hormone-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders. Intestinal nutrient-sensing is important in metabolic control. Here the authors show that the gut-derived hormone Allatostatin C, a somatostatin homolog in fruit flies, links enteric nutrient sensing to behavioral and metabolic adaptations that maintain energetic homeostasis in Drosophila melanogaster.

More than half of all extant metazoan species on earth are insects. The evolutionary success of insects is linked with their ability to osmoregulate, suggesting that they have evolved unique physiological mechanisms to maintain water balance. In beetles (Coleoptera)—the largest group of insects—a specialized rectal (“cryptonephridial”) complex has evolved that recovers water from the rectum destined for excretion and recycles it back to the body. However, the molecular mechanisms underpinning the remarkable water-conserving functions of this system are unknown. Here, we introduce a transcriptomic resource, BeetleAtlas.org, for the exceptionally desiccation-tolerant red flour beetle Tribolium castaneum, and demonstrate its utility by identifying a cation/H⁺ antiporter (NHA1) that is enriched and functionally significant in the Tribolium rectal complex. NHA1 localizes exclusively to a specialized cell type, the leptophragmata, in the distal region of the Malpighian tubules associated with the rectal complex. Computational modeling and electrophysiological characterization in Xenopus oocytes show that NHA1 acts as an electroneutral K⁺/H⁺ antiporter. Furthermore, genetic silencing of Nha1 dramatically increases excretory water loss and reduces organismal survival during desiccation stress, implying that NHA1 activity is essential for maintaining systemic water balance. Finally, we show that Tiptop, a conserved transcription factor, regulates NHA1 expression in leptophragmata and controls leptophragmata maturation, illuminating the developmental mechanism that establishes the functions of this cell. Together, our work provides insights into the molecular architecture underpinning the function of one of the most powerful water-conserving mechanisms in nature, the beetle rectal complex.

Animals maintain metabolic homeostasis by modulating the activity of specialized organs that adjust internal metabolism to external conditions. However, the hormonal signals coordinating these functions are incompletely characterized. Here we show that six neurosecretory cells in the Drosophila central nervous system respond to circulating nutrient levels by releasing Capa hormones, homologs of mammalian neuromedin U, which activate the Capa receptor (CapaR) in peripheral tissues to control energy homeostasis. Loss of Capa/CapaR signaling causes intestinal hypomotility and impaired nutrient absorption, which gradually deplete internal nutrient stores and reduce organismal lifespan. Conversely, increased Capa/CapaR activity increases fluid and waste excretion. Furthermore, Capa/CapaR inhibits the release of glucagon-like adipokinetic hormone from the corpora cardiaca, which restricts energy mobilization from adipose tissue to avoid harmful hyperglycemia. Our results suggest that the Capa/CapaR circuit occupies a central node in a homeostatic program that facilitates the digestion and absorption of nutrients and regulates systemic energy balance. Maintaining metabolic homeostasis during feeding and fasting states is critical to animal survival. Here the authors show that Capa hormone signaling, homologs to mammalian Neuromedin U, helps control homeostasis via regulation of nutrient uptake and energy storage in Drosophila.

The increasing incidence of extreme wildfire is becoming a concern for public health. Although long-term exposure to wildfire smoke is associated with respiratory illnesses, reports on the association between short-term occupational exposure to wildfire smoke and lung function remain scarce. In this cross-sectional study, we analyzed data from 218 Royal Canadian Mounted Police officers (mean age: 38 ± 9 years) deployed at the Fort McMurray wildfires in 2016. Individual exposure to air pollutants was calculated by integrating the duration of exposure with the air quality parameters obtained from the nearest air quality monitoring station during the phase of deployment. Lung function was measured using spirometry and body plethysmography. Association between exposure and lung function was examined using principal component linear regression analysis, adjusting for potential confounders. In our findings, the participants were predominantly male (71%). Mean forced expiratory volume in 1 s (FEV1), and residual volume (RV) were 76.5 ± 5.9 and 80.1 ± 19.5 (% predicted). A marginal association was observed between air pollution and higher RV [β: 1.55; 95% CI: −0.28 to 3.37 per interquartile change of air pollution index], but not with other lung function indices. The association between air pollution index and RV was significantly higher in participants who were screened within the first three months of deployment (2.80; 0.91 to 4.70) than those screened later (−0.28; −2.58 to 2.03), indicating a stronger effect of air pollution on peripheral airways. Acute short-term exposure to wildfire-associated air pollutants may impose subtle but clinically important deleterious respiratory effects, particularly in the peripheral airways.

Many insulating materials are used in construction, although few have been reported to cause non-malignant respiratory illnesses. We aimed to investigate associations between exposures to insulating materials and non-malignant respiratory illnesses in insulators. In this cross-sectional study, 990 insulators (45 ± 14 years) were screened from 2011–2017 in Alberta. All participants underwent pulmonary function tests and chest radiography. Demographics, work history, and history of chest infections were obtained through questionnaires. Chronic obstructive pulmonary disease (COPD) was diagnosed according to established guidelines. Associations between exposures and respiratory illnesses were assessed by modified Poisson regression. Of those screened, 875 (88%) were males. 457 (46%) participants reported having ≥ 1 chest infection in the past 3 years, while 156 (16%) were diagnosed with COPD. In multivariate models, all materials (asbestos, calcium silicate, carbon fibers, fiberglass, and refractory ceramic fibers) except aerogels and mineral fibers were associated with recurrent chest infections (prevalence ratio [PR] range: 1.18–1.42). Only asbestos was associated with COPD (PR: 1.44; 95% confidence interval [CI]: 1.01, 2.05). Therefore, occupational exposure to insulating materials was associated with non-malignant respiratory illnesses, specifically, recurrent chest infections and COPD. Longitudinal studies are urgently needed to assess the risk of exposure to these newly implemented insulation materials.

Abstract The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the specific gut hormones that communicate energy availability to target organs to induce appropriate metabolic and behavioral responses are poorly defined. Here we show that the enteroendocrine cells (EECs) of the Drosophila gut sense nutrient stress via the intracellular TOR pathway, and in response secrete the peptide hormone allatostatin C (AstC). Gut-derived AstC induces secretion of glucagon-like adipokinetic hormone (AKH) via its receptor AstC-R2, a homolog of mammalian somatostatin receptors, to coordinate food intake and energy mobilization. Loss of gut AstC or its receptor in the AKH-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders. Competing Interest Statement The authors have declared no competing interest.

The regulation of systemic energy balance involves the coordinated activity of specialized organs, which control nutrient uptake, utilization and storage to promote metabolic homeostasis during environmental challenges. The humoral signals that drive such homeostatic programs are largely unidentified. Here we show that three pairs of central neurons in adult Drosophila respond to internal water and nutrient availability by releasing Capa-1 and -2 hormones that signal through the Capa receptor (CapaR) to exert systemic metabolic control. Loss of Capa/CapaR signaling leads to intestinal hypomotility and impaired nutrient absorption, which gradually deplete internal nutrient stores and reduce organismal lifespan. Conversely, hyperactivation of the Capa circuitry stimulates fluid and waste excretion. Furthermore, we demonstrate that Capa/CapaR regulates energy metabolism by modulating the release of the glucagon-like adipokinetic hormone, which governs lipolysis in adipose tissue to stabilize circulating energy levels. Altogether, our results uncover a novel inter-tissue program that plays a central role in coordinating post-prandial responses that are essential to maintain adult viability. Competing Interest Statement The authors have declared no competing interest.

Tenebrionid beetles have been highly successful in colonising environments where water is scarce, underpinned by their unique osmoregulatory adaptations. These include a cryptonephridial arrangement of their organs, in which part of their renal/Malpighian tubules are bound to the surface of the rectum. This allows them to generate a steep osmotic gradient to draw water from within the rectum and return it to the body. Within the cryptonephridial tubules a seemingly novel cell type, the leptophragmata, is considered to play a key role in transporting potassium chloride to generate this osmotic gradient. Nothing was known about the developmental mechanisms or evolution of these unusual renal cells. Here we investigate the mechanisms underpinning development of the leptophragmata in the red flour beetle, Tribolium castaneum. We find that leptophragmata express and require a teashirt/tiptop transcription factor gene, as do the secondary renal cells of Drosophila melanogaster which lack a cryptonephridial arrangement. We also find an additional transcription factor, Dachshund, is required to establish leptophragmata identity and to distinguish them from the secondary cells in Tribolium's non-cryptonephridial region of renal tubule. Dachshund is also expressed in a sub-population of secondary cells in Drosophila. So leptophragmata, which are unique to the beetle lineage, appear to have originated from a specific renal cell type present ancestrally, and specified by a conserved repertoire of transcription factors.Competing Interest StatementThe authors have declared no competing interest.

We investigate the thermodynamic consistency of the master equation description of heat transport through an optomechanical system attached to two heat baths, one optical and one mechanical. We employ three different master equations to describe this scenario: (i) The standard master equation used in optomechanics, where each bath acts only on the resonator that it is physically connected to; (ii) the so-called dressed-state master equation, where the mechanical bath acts on the global system; and (iii) what we call the global master equation, where both baths are treated non-locally and affect both the optical and mechanical subsystems. Our main contribution is to demonstrate that, under certain conditions including when the optomechanical coupling strength is weak, the second law of thermodynamics is violated by the first two of these pictures. In order to have a thermodynamically consistent description of an optomechanical system, therefore, one has to employ a global description of the effect of the baths on the system.