bioRxiv - Physiology最新文献

{"title":"Diurnal regulation of Acyl-CoA synthetase 3 (ACSF3) underlies daily mitochondrial lysine-malonylation and hepatic metabolism","authors":"Enora LeQuestel, Charlene Besnard, Florian Atger, Yolene Foucher, Alwena Tollec, Victoria Pakulska, Arsenio Rodrigues Oliveira, Chloe Clotteau, Mathilde Gourdel, Ivan Nemazanyy, Mikael Croyal, Yohann Coute, David Jacobi, Bertrand Cariou, Daniel Mauvoisin","doi":"10.1101/2024.09.03.607283","DOIUrl":"https://doi.org/10.1101/2024.09.03.607283","url":null,"abstract":"Circadian rhythms are fundamental to maintaining health and are implicated in various diseases. In the liver, daily rhythms are coordinated via the interplay between feeding rhythms and the molecular circadian clock, ensuring metabolic homeostasis. Disruption of feeding rhythms can lead to circadian misalignment, contributing to metabolic disorders, yet the underlying molecular mechanisms remain unclear. Recent evidence suggests that post-translational modifications play a key role in regulating circadian functional output. In this framework, mitochondria serve as a convergence point, integrating rhythms in metabolism, feeding rhythms and the circadian clock. In the present study, we used a multi-omics approach to investigate the role of the Acyl-CoA synthetase 3 (ACSF3) in driving lysine-malonylation and in regulating daily hepatic metabolism. We found that ACSF3 expression and its mediated impact on lysine-malonylation are rhythmic and largely governed by feeding rhythms. While hepatic ACSF3 knockdown did not alter diet-induced metabolic abnormalities, our results demonstrate that ACSF3 plays a role in the diurnal regulation of liver glycogen storage, de novo lipogenesis, and triglyceride synthesis.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary zinc restriction mimics protein restriction and extends lifespan in Drosophila","authors":"Hina Kosakamoto, Hide Aikawa, Souto Kitazawa, Chisako Sakuma, Rina Okada, Masayuki Miura, Fumiaki Obata","doi":"10.1101/2024.08.28.610190","DOIUrl":"https://doi.org/10.1101/2024.08.28.610190","url":null,"abstract":"Dietary restriction extends lifespan in model organisms, mainly through dietary amino acids. Compared to macronutrients, the effect of dietary micronutrients on organismal lifespan has not been intensively investigated. Here, using a synthetic diet, we test whether restriction of each micronutrient, including vitamins and minerals, affects lifespan and fecundity in adult Drosophila. While restriction of many of these micronutrients have either negative or no impact on lifespan, zinc (Zn) restriction alone can increase it. Dietary Zn restriction (ZnR) decreases fecundity, increases starvation resistance, and promotes preference for feeding amino acids, in adult females, phenocopying dietary amino acid restriction. Our study demonstrates that dietary intake of trace elements has profound impacts on physiology and lifespan, and that limiting dietary zinc may be a strategy to improve the healthspan of animals.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subunit-specific conductance of single HCN pacemaker channels at femtosiemens resolution","authors":"Klaus Benndorf, Uta Enke, Debanjan Tewari, Jana Kusch, Haoran Liu, Han Sun, Ralf Schmauder, Christian Sattler","doi":"10.1101/2024.09.02.610748","DOIUrl":"https://doi.org/10.1101/2024.09.02.610748","url":null,"abstract":"Hyperpolarization-activated cyclic nucleotide-modulated (HCN) channels are tetramers that generate rhythmic electrical activity in neuronal and cardiac pacemaker cells. The channels are activated by hyperpolarisation of the membrane voltage and additionally tuned by the second messenger cAMP at sympathetic stimulation. There are four mammalian isoforms, HCN 1-4. The single-channel conductance, gamma, of HCN channels remains debated, with conflicting results ranging from near 1.5 pS for HCN2 to tens of pS for HCN1, HCN2 and HCN4, though the pore structure, viewed to determine the conductance, is either identical or highly conserved. To resolve this controversy, we analyzed all four mouse isoforms mHCN1-4 at femtosiemens resolution. We show that mHCN1, mHCN3 and mHCN4 also generate small conductance values, even smaller than that of mHCN2 with the sequence gamma mHCN2=1.54 pS > gamma mHCN1=0.84 pS > gamma mHCN3=0.54 pS approx gamma mHCN4=0.51 pS. As shown by systematic mutagenesis and molecular dynamic simulations, the differences in the conductance are neither generated by the selectivity filter nor the inner gate, but by defined negative charges in the outer channel vestibule increasing cation occupation. In line with these results, heteromers of mHCN2 with either mHCN1, mHCN3 or mHCN4 lead to graded single-channel currents in-between those of the respective homomeric channels. Our approach at femtosiemens resolution provides insight into the function of recombinant and native HCN channels at the level of single subunits and is thus promising for the development of subunit-specific drugs acting on these clinically highly relevant channels.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early brain neuroinflammatory and metabolic changes identified by dual tracer microPET imaging in mice with acute liver injury","authors":"Santhoshi Palandira, Aidan Falvey, Joseph Carrion, Qiong Zeng, Saher Chaudhry, Kira Grossman, Lauren Turecki, Nha Nguyen, Michael Brines, Sangeeta S. Chavan, Christine N. Metz, Yousef Al-Abed, Eric H. Chang, Yilong Ma, David Eidelberg, An Vo, Kevin J. Tracey, Valentin A. Pavlov","doi":"10.1101/2024.09.02.610840","DOIUrl":"https://doi.org/10.1101/2024.09.02.610840","url":null,"abstract":"Background Acute liver injury (ALI) that progresses into acute liver failure (ALF) is a life-threatening condition with an increasing incidence and associated costs. Acetaminophen (N-acetyl-p-aminophenol, APAP) overdosing is among the leading causes of ALI and ALF in the Northern Hemisphere. Brain dysfunction defined as hepatic encephalopathy is one of the main diagnostic criteria for ALF. While neuroinflammation and brain metabolic alterations significantly contribute to hepatic encephalopathy, their evaluation at early stages of ALI remained challenging. To provide insights, we utilized post-mortem analysis and non-invasive brain micro positron emission tomography (microPET) imaging of mice with APAP-induced ALI. Methods Male C57BL/6 mice were treated with vehicle or APAP (600 mg/kg, i.p.). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver damage (using H&E staining), hepatic and serum IL-6 levels, and hippocampal IBA1 (using immunolabeling) were evaluated at 24h and 48h. Vehicle and APAP treated animals also underwent microPET imaging utilizing a dual tracer approach, including [11C]-peripheral benzodiazepine receptor ([11C]PBR28) to assess microglia/astrocyte activation and [18F]-fluoro-2-deoxy-2-D-glucose ([18F]FDG) to assess energy metabolism. Brain images were pre-processed and evaluated using conjunction and individual tracer uptake analysis. Results APAP-induced ALI and hepatic and systemic inflammation were detected at 24h and 48h by significantly elevated serum ALT and AST levels, hepatocellular damage, and increased hepatic and serum IL-6 levels. In parallel, increased microglial numbers, indicative for neuroinflammation were observed in the hippocampus of APAP-treated mice. MicroPET imaging revealed overlapping increases in [11C]PBR28 and [18F]FDG uptake in the hippocampus, thalamus, and habenular nucleus indicating microglial/astroglial activation and increased energy metabolism in APAP-treated mice (vs. vehicle-treated mice) at 24h. Similar significant increases were also found in the hypothalamus, thalamus, and cerebellum at 48h. The individual tracer uptake analyses (APAP vs vehicle) at 24h and 48h confirmed increases in these brain areas and indicated additional tracer- and region-specific effects including hippocampal alterations. Conclusion Peripheral manifestations of APAP-induced ALI in mice are associated with brain neuroinflammatory and metabolic alterations at relatively early stages of disease progression, which can be non-invasively evaluated using microPET imaging and conjunction analysis. These findings support further PET-based investigations of brain function in ALI/ALF that may inform timely therapeutic interventions.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pvf1-PvR-mediated crosstalk between the trachea and the gut guides intestinal stem cell migration to promote gut regeneration.","authors":"Duncan John MacKay, Alphy John, Christian F Christensen, Rihab Loudhaief, Abdul B Tanari, Matteo Rauzi, Julien Colombani, Ditte S Andersen","doi":"10.1101/2024.09.02.609652","DOIUrl":"https://doi.org/10.1101/2024.09.02.609652","url":null,"abstract":"In adult tissues, stem cells (SCs) reside in specialized niches, where they are maintained in a quiescent state until activated by injury. Once activated, they migrate towards injured sites, where they proliferate and differentiate to replenish lost or damaged cells. Although effective tissue repair relies critically on the ability of SCs to reach and populate damaged sites, mechanisms guiding SCs towards these sites are not well understood. This is largely due to the technical challenges involved in monitoring SC dynamics in real time in vivo. Here, we devised an experimental framework that allows for real-time tracking of the spatiotemporal dynamics of intestinal SCs (ISCs) during the early phases of gut regeneration. Our data show that ISC migration is rapidly induced following injury and precedes ISC divisions and differentiation. We identify the Drosophila PDGF-VEGF-related receptor, Pvr, as a critical regulator of the migratory response to epithelial damage. ISC-specific Pvr depletion strongly suppresses ISC migration towards affected sites as well as the regenerative response. We further show that the Pvr ligand, PDGF-VEGF-related factor 1 (Pvf1), is produced by the trachea/vasculature in response to intestinal damage and acts as a guidance signal to direct ISC migration towards affected areas. Our work highlights a critical role of gut-trachea/vasculature crosstalk in guiding ISC migration during regeneration. As neovascularization of injured sites is a key feature of tissue repair in both flies and mammals, these findings could be relevant to regenerative processes in a wide range of adult tissues.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diurnal variation in skeletal muscle mitochondrial function dictates time of day-dependent differences in exercise capacity","authors":"Subhash Khatri, Souparno Das, Anshit Singh, Shabbir Ahmed, Mohit Kashiv, Sunil Laxman, Ullas Kolthur-Seetharam","doi":"10.1101/2024.09.02.610727","DOIUrl":"https://doi.org/10.1101/2024.09.02.610727","url":null,"abstract":"Exercise impinges on almost all physiological processes at an organismal level and is a potent intervention to treat various diseases. Exercise performance is well established to display diurnal rhythm, peaking during the late active phase. However, the underlying molecular/metabolic factors and mitochondrial energetics that possibly dictate time-of-day exercise capacity remain unknown. Here, we have unraveled the importance of diurnal variation in mitochondrial functions as a determinant of skeletal muscle exercise performance. Our results show that exercise-induced muscle metabolome and energetics are distinct at ZT3 and ZT15. Importantly, we have elucidated key diurnal differences in mitochondrial functions that are well correlated with disparate time-of-day dependent exercise capacity. Providing causal evidence, we illustrate that loss of Sirtuin4 (SIRT4), a well-known mitochondrial regulator, abrogates diurnal variation in mitochondrial functions and consequently abolishes time-of-day dependent exercise performance. Therefore, our findings unequivocally demonstrate the pivotal role of baseline skeletal-muscle mitochondrial functions in dictating diurnal exercise capacity.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pain distribution can be determined by classical conditioning","authors":"Jakub Nastaj, Jacek Skalski, Daria Nowak, Natalia Kruszyna, Przemyslaw Babel, Tibor Szikszay, Kerstin Luedtke, Rafal Gnat, Waclaw M. Adamczyk","doi":"10.1101/2024.08.31.609921","DOIUrl":"https://doi.org/10.1101/2024.08.31.609921","url":null,"abstract":"ABSTRACT\u0000Chronic widespread pain (CWP) - as many other clinical presentations - manifests in ongoing pain without identifiable structural cause, with pain that spreads over multiple body areas. The development and maintenance of symptoms may involve learning mechanisms. The authors have hypothesized that pain distribution can be learned through classical conditioning or elicited by verbal suggestion. Ninety-four healthy volunteers participated in this study and were randomly distributed to four groups. In the classical conditioning combined with verbal suggestion group, US- (small pain distribution) and US+ (large pain distribution) were paired with visual stimuli (CS+ and CS-) and participants were told about this association. In the verbal suggestion group, the conditioning was not performed, whereas in classical conditioning only group, learning was not combined with suggestion. In the control group, conditioning and suggestion did not take place. Ratings of perceived pain distribution (PD) were collected after each trial and ratings of pain intensity after each block of trials. During the testing phase, participants were exposed to electrocutaneous stimuli corresponding to only the small (US-) pain distribution. Results showed significant differences between CS+ and CS- pain distribution ratings across the experimental groups: conditioning + verbal suggestion (p<0.01), conditioning only group (p<0.05) and verbal suggestion only group (p<0.05), but not in the control group (p>0.05). Furthermore, significant differences in the perceived pain distribution were found between the control group and all experimental groups. This result supports our main hypothesis that the perceived pain distribution can be influenced by classical conditioning as well as verbal suggestion, although the effect is stronger when both are combined. Key words: pain, classical conditioning, pain distribution, spatial aspect of pain, learning mechanism","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"207 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translation components in adult Drosophila melanogaster adipocytes regulate the ovarian germline stem cell lineage","authors":"Subhshri Sahu, Alissa Richmond Armstrong","doi":"10.1101/2024.08.31.610632","DOIUrl":"https://doi.org/10.1101/2024.08.31.610632","url":null,"abstract":"Adult stem cells, which support tissue homeostasis and damage repair, are influenced by whole organism physiology. Dietary input has a major impact on the stem cell supported ovary in Drosophila melanogaster females, appropriately matching reproductive output to nutrient availability. Previous work has shown that inter-organ communication plays a role in modulating the ovarian response to diet. Specifically, amino acid sensing by the adipose tissue remotely controls germline stem cells and their progeny. While we have shown that activation of the amino acid response pathway, a part of the integrated stress response, and mTOR signaling in adipocytes impacts germline stem cell maintenance and ovulation, it is unclear how downstream signaling mediates these responses. Here, using a combination of genetic and cell biological tools, we show that regulation of translation in adult adipocytes impacts the ovarian germline stem cell lineage, from stem cell maintenance to ovulation of mature oocytes. This work strongly suggests that the adipose tissue produces specific factors to control stem cell activity in the ovary and highlights how inter-organ communication underlies organismal physiological responses to diet.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ketone Body Metabolism is Not Required for Improvement of Heart Failure by Ketogenic Diet in Mice","authors":"Zachary Foulks, Carla J Weinheimer, Attila Kovacs, Jessica Michael, Kelly D Pyles, Thiago N Menezes, Kevin Cho, Gary J Patti, Kyle S McCommis","doi":"10.1101/2024.08.30.610511","DOIUrl":"https://doi.org/10.1101/2024.08.30.610511","url":null,"abstract":"Failing hearts increasingly metabolize ketone bodies, and enhancing ketosis improves heart failure (HF) remodeling. Circulating ketones are elevated by fasting/starvation, which is mimicked with a high-fat, low-carbohydrate ketogenic diet (KD). While speculated that KD improves HF through increased ketone oxidation, some evidence suggests KD paradoxically downregulates cardiac ketone oxidation despite increased ketone delivery. We sought to clarify the significance of cardiac ketone metabolism during KD in HF. Mice were subjected to transverse aortic constriction with apical myocardial infarction (TAC-MI) and fed either low-fat (LF) control or KD. Cardiac-specific mitochondrial pyruvate carrier 2 (csMPC2-/-) mice were used as a second model of heart failure. In both mice, feeding a KD improved HF, determined by echocardiography, heart weights, and gene expression analyses. Although KD increases plasma ketone bodies, gene expression for ketone metabolic genes is decreased in the hearts of KD-fed mice. Cardiac-specific β-hydroxybutyrate dehydrogenase 1 (csBDH1-/-), the first enzyme in ketone catabolism, mice were also studied and crossed with the csMPC2-/- mice to create double knockout (DKO) mice. These mice were aged to 16 weeks and switched to LF or KD, and KD was able to completely normalize the hearts of both csMPC2-/- and DKO mice, suggesting that ketone metabolism is unnecessary for improving heart failure with ketogenic diet. These studies were then repeated, and mice injected with U-13C-β-hydroxybutyrate to evaluate ketone metabolism. KD feeding significantly decreased the enrichment of the TCA cycle from ketone body carbons, as did the BDH1-deletion in DKO mice. Gene expression and respirometry suggests that KD instead increases cardiac fat oxidation. In conclusion, these results suggest that ketogenic diet decreases cardiac ketone metabolism and does not require ketone metabolism to improve heart failure.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"71 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Consumption of human-relevant levels of sucrose-water rewires macronutrient uptake and utilization mechanisms in a tissue specific manner","authors":"Saptarnab Ganguly, Tandrika Chattopadhyay, Rubina Kazi, SOuparno Das, Bhavisha Malik, Uthpala ML, Padmapriya Shankar Iyer, Mohit Kashiv, Anshit Singh, Amita Ghadge, Shyam Nair, Mahendra Sonawane, Ullas Kolthur-Seetharam","doi":"10.1101/2024.08.31.610015","DOIUrl":"https://doi.org/10.1101/2024.08.31.610015","url":null,"abstract":"Consumption of sugar-sweetened beverages (SSBs) have been linked to metabolic dysfunction, obesity, diabetes and enhanced risk of cardiovascular diseases across all age-groups globally. Decades of work that have provided insights into pathophysiological manifestations of sucrose overfeeding have employed paradigms that rarely mimic human consumption of SSBs. Thus, our understanding of multi-organ cross-talk and molecular and/or cellular mechanisms, which operate across scales and drive physiological derangement is still poor. By employing a\u0000paradigm of sucrose water feeding in mice that closely resembles chronic SSB consumption in humans (10% sucrose in water), we have unraveled hitherto unknown tissue-specific mechanistic underpinnings, which contribute towards perturbed physiology. Our findings illustrate that systemic impaired glucose homeostasis, mediated by hepatic gluconeogenesis and insulin resistance, does not involve altered gene expression programs in the liver. We have discovered the pivotal role of the small intestine, which in conjunction with liver and muscles, drives dyshomeostasis. Importantly, we have uncovered rewiring of molecular mechanisms in the proximal intestine that is either causal or consequential to systemic ill-effects of chronic sucrose water consumption including dysfunction of liver and muscle mitochondria. Tissue-specific molecular signatures, which we have unveiled, clearly indicate that inefficient utilization of glucose is exacerbated by enhanced uptake by the gut. Besides providing systems-wide mechanistic insights, we propose that consumption of SSBs causes intestinal molecular addiction for deregulated absorption of hexose-sugars, and drives diseases such as diabetes and obesity.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}