Acta Physiologica最新文献

{"title":"Physical activity and sedentary behavior show distinct associations with tissue-specific insulin sensitivity in adults with overweight","authors":"Lisa Wanders,&nbsp;Anouk Gijbels,&nbsp;Esmée A. Bakker,&nbsp;Inez Trouwborst,&nbsp;Kelly M. Jardon,&nbsp;Koen C. M. Manusama,&nbsp;Gabby B. Hul,&nbsp;Edith J. M. Feskens,&nbsp;Lydia A. Afman,&nbsp;Ellen E. Blaak,&nbsp;Maria T. E. Hopman,&nbsp;Gijs H. Goossens,&nbsp;Dick H. J. Thijssen","doi":"10.1111/apha.13945","DOIUrl":"https://doi.org/10.1111/apha.13945","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The aim of this study is to investigate associations between the physical activity (PA) spectrum (sedentary behavior to exercise) and tissue-specific insulin resistance (IR).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We included 219 participants for analysis (median [IQR]: 61 [55; 67] years, BMI 29.6 [26.9; 32.0] kg/m²; 60% female) with predominant muscle or liver IR, as determined using a 7-point oral glucose tolerance test (OGTT). PA and sedentary behavior were measured objectively (ActivPAL) across 7 days. Context-specific PA was assessed with the Baecke questionnaire. Multiple linear regression models (adjustments include age, sex, BMI, site, season, retirement, and dietary intake) were used to determine associations between the PA spectrum and hepatic insulin resistance index (HIRI), muscle insulin sensitivity index (MISI) and whole-body IR (HOMA-IR, Matsuda index).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In fully adjusted models, objectively measured total PA (standardized regression coefficient <i>β</i> = 0.17, <i>p</i> = 0.020), light-intensity PA (<i>β</i> = 0.15, <i>p</i> = 0.045) and moderate-to-vigorous intensity PA (<i>β</i> = 0.13, <i>p</i> = 0.048) were independently associated with Matsuda index, but not HOMA-IR (<i>p</i> &gt; 0.05). A higher questionnaire-derived sport index and leisure index were associated with significantly lower whole-body IR (Matsuda, HOMA-IR) in men but not in women. Results varied across tissues: more time spent sedentary (<i>β</i> = −0.24, <i>p</i> = 0.045) and a higher leisure index (<i>β</i> = 0.14, <i>p</i> = 0.034) were respectively negatively and positively associated with MISI, but not HIRI. A higher sport index was associated with lower HIRI (<i>β</i> = −0.30, <i>p</i> = 0.007, in men only).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>While we confirm a beneficial association between PA and whole-body IR, our findings indicate that associations between the PA spectrum and IR seem distinct depending on the primary site of insulin resistance (muscle or liver).</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13945","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6111421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian rhythms in auditory hallucinations and psychosis","authors":"Hong-Viet V. Ngo,&nbsp;Henrik Oster,&nbsp;Christina Andreou,&nbsp;Jonas Obleser","doi":"10.1111/apha.13944","DOIUrl":"https://doi.org/10.1111/apha.13944","url":null,"abstract":"<p>Circadian rhythms are imprinted in all organisms and influence virtually all aspects of physiology and behavior in adaptation to the 24-h day–night cycle. This recognition of a circadian timekeeping system permeating essentially all healthy functioning of body and mind quickly leads to the realization that, in turn, human ailments should be probed for the degree to which they are rooted in or marked by disruptions and dysregulations of circadian clock functions in the human body. In this review, we will focus on psychosis as a key mental illness and foremost one of its cardinal symptoms: auditory hallucinations. We will discuss recent empirical evidence and conceptual advances probing the potential role of circadian disruption in auditory hallucinations. Moreover, a dysbalance in excitation and inhibition within cortical networks, which in turn drive a disinhibition of dopaminergic signaling, will be highlighted as central physiological mechanism. Finally, we will propose two avenues for experimentally intervening on the circadian influences to potentially alleviate hallucinations in psychotic disorders.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13944","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6146723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A single dose of exercise stimulates skeletal muscle mitochondrial plasticity in myotonic dystrophy type 1","authors":"Andrew I. Mikhail,&nbsp;Alexander Manta,&nbsp;Sean Y. Ng,&nbsp;Aislin K. Osborne,&nbsp;Stephanie R. Mattina,&nbsp;Mark R. Mackie,&nbsp;Vladimir Ljubicic","doi":"10.1111/apha.13943","DOIUrl":"https://doi.org/10.1111/apha.13943","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Myotonic dystrophy type 1 (DM1) is the second most common muscular dystrophy after Duchenne and is the most prevalent muscular dystrophy in adults. DM1 patients that participate in aerobic exercise training experience several physiological benefits concomitant with improved muscle mitochondrial function without alterations in typical DM1-specific disease mechanisms, which suggests that correcting organelle health is key to ameliorate the DM1 pathology. However, our understanding of the molecular mechanisms of mitochondrial turnover and dynamics in DM1 skeletal muscle is lacking.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Skeletal muscle tissue was sampled from healthy and DM1 mice under sedentary conditions and at several recovery time points following an exhaustive treadmill run.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We demonstrate that DM1 patients exhibit an imbalance in the transcriptional apparatus for mitochondrial turnover and dynamics in skeletal muscle. Additionally, DM1 mice displayed elevated expression of autophagy and mitophagy regulators. A single dose of exercise successfully enhanced canonical exercise molecular pathways and skeletal muscle mitochondrial biogenesis despite failing to alter the cellular pathology in DM1 mice. However, treadmill running stimulated coordinated organelle fusion and fission signaling, as well as improved alternative splicing of <i>Optic atrophy 1</i>. Exercise also evoked autophagy and mitophagy pathways in DM1 skeletal muscle resulting in the normalized expression of autophagy- and lysosome-related machinery responsible for the clearance of dysfunctional organelles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Collectively, our data indicate that mitochondrial dynamics and turnover processes in DM1 skeletal muscle are initiated with a single dose of exercise, which may underlie the adaptive benefits previously documented in DM1 mice and patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13943","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5648571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An update on hypertension","authors":"Ralf Mrowka","doi":"10.1111/apha.13942","DOIUrl":"https://doi.org/10.1111/apha.13942","url":null,"abstract":"&lt;p&gt;Arterial hypertension is a serious medical condition that significantly increases the risks of heart, brain, kidney, and other diseases affecting 1.28 billion adults worldwide. Hypertension is a major cause of premature death worldwide. This pathological condition is also called a “silent killer.” Most people with hypertension are unaware of the problem because it may have no symptoms until the first complications occur. This is why it is so important that blood pressure is measured on a regular basis.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;The aim of the following contribution is to highlight some of recent papers that appeared in &lt;i&gt;Acta Physiologica&lt;/i&gt; with focus on articles that might be of importance to the field of arterial hypertension research and related topics. The scope that was covered in this field in &lt;i&gt;Acta Physiologica&lt;/i&gt; ranged from basic research conducted in animal models to studies closely related to clinical questions.&lt;/p&gt;&lt;p&gt;Form a historic perspective, comparative physiology models have been a hallmark of studies on animal osmoregulation.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; The basic idea is that animal experiments might be used to study fundamental mechanisms that are involved also in humans in the following particular example case for mechanisms relating to blood pressure regulation such as sodium and potassium transporters. In this specific case Clifford &lt;i&gt;et al&lt;/i&gt;&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; determined whether Na+ uptake in adult zebrafish (Danio rerio) exposed to acidic water adheres to traditional models reliant on Na+/H+ Exchangers (NHEs), Na+ channels and Na+/Cl− Cotransporters (NCCs) or if it might occur through a novel mechanism. In order to achieve this the zebrafish were exposed to control or acidic (pH 4.0) water for 0–12 h during which radioactive Na+ uptake, ammonia excretion, net acidic equivalent flux, and net K+ flux were measured. The involvement of the possible transporters was evaluated by exposure to Cl− -free or elevated [K+] water, or to pharmacological inhibitors. The presence of NCKXs in gill was examined using RT-PCR. The authors found that the uptake of sodium was strongly attenuated by acid exposure, but gradually recovered to control rates. The systematic elimination of each of the traditional models led the authors to consider K+ as a counter substrate for Na+ uptake during acid exposure. The elevated environmental potassium inhibited sodium uptake during acid exposure in a concentration-dependent manner. Analysis of mRNA revealed that six NCKX isoforms were present in zebrafish gills. The main conclusion of this article is that during acid exposure, zebrafish engage a novel Na+ uptake mechanism that utilizes the outwardly directed K+ gradient as a counter-substrate for Na+ and is sensitive to tetraethylammonium. NKCXs are promising candidates to mediate this potassium-dependent sodium uptake.&lt;/p&gt;&lt;p&gt;How these findings relate to human physiology remains to be determined. One possible approach is to check wheth","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 3","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13942","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6097171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alarm off: Maintained kidney tissue oxygen tension when mobilizing GFR reserve","authors":"Boye L. Jensen","doi":"10.1111/apha.13941","DOIUrl":"https://doi.org/10.1111/apha.13941","url":null,"abstract":"&lt;p&gt;In the current issue of &lt;i&gt;Acta Physiologica&lt;/i&gt;, Jufar et al&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; address the coupling between changes in glomerular filtration rate and kidney tissue oxygenation. This relation gains increased attention not least due to the demonstration that blocking transepithelial transport in humans by, for example, the loop diuretic furosemide may increase kidney tissue oxygen tension and lower consumption.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; The assumption is that sudden increases in GFR would be followed by proportional increases in tubular epithelial transport workload and oxygen consumption. This could potentially lead to lower tissue oxygen tension if not balanced by an increase in renal blood flow and particularly in the medulla where blood supply is limited. Jufar et al&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; elegantly exploit in vivo techniques to directly measure kidney regional oxygen tension in a large animal model (sheep). Infusion of a mixture of amino acids, a classic maneuver to mobilize renal reserve capacity, resulted in an increase in GFR (40%), renal blood flow and oxygen supply accompanied by increased oxygen consumption. Of novelty was the insertion of dual-fiber optic probes in tissue to record tissue O&lt;sub&gt;2&lt;/sub&gt; tension, temperature, and flow with validation of placement post hoc. Cortex and medulla tissue oxygenation did not decrease but rather increased in response to amino acid infusion. Authors conclude that in healthy adult sheep, the mobilization of renal reserve capacity, at least by amino acid infusion, with documented increase in sodium reabsorption, does not threaten kidney tissue oxygenation in this acute setting.&lt;/p&gt;&lt;p&gt;As always using a complex in vivo setting, several interpretations and confounders must be taken into consideration before extrapolating safely to more chronic and human settings. The study raises several interesting questions. Renal functional reserve denotes the ability to increase GFR above and beyond baseline. This can be done experimentally and diagnostically in humans by, for example, dopamine infusion, increased protein intake/amino acid infusion (as used here) and is seen, more dramatically, in the remaining kidney following donation of one kidney or cancer nephrectomy. In physiological settings, pregnancy is a situation where GFR increases above normal and in pathophysiology, early diabetes is associated with increased GFR. These situations are quite different but are characterized by different degrees of increased renal blood flow and likely by differential changes in glomerular arteriolar resistances. Amino acid infusion is thought to, at least partially, rely on attenuated tubuloglomerular feedback (TGF), similarly to early diabetes and high protein intake. Increased filtration of amino acids (or glucose in diabetes) will increase proximal reabsorption of Na&lt;sup&gt;+&lt;/sup&gt; and lower tubular NaCl concentration at the macula densa leading to afferent arteriolar dilatation. A specific feature of the am","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6068906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple sclerosis and circadian rhythms: Can diet act as a treatment?","authors":"Olga Pivovarova-Ramich,&nbsp;Hanna Gwendolyn Zimmermann,&nbsp;Friedemann Paul","doi":"10.1111/apha.13939","DOIUrl":"https://doi.org/10.1111/apha.13939","url":null,"abstract":"<p>Multiple sclerosis (MS) is an autoimmune inflammatory and neurodegenerative disease of the central nervous system (CNS) with increasing incidence and prevalence. MS is associated with inflammatory and metabolic disturbances that, as preliminary human and animal data suggest, might be mediated by disruption of circadian rhythmicity. Nutrition habits can influence the risk for MS, and dietary interventions may be effective in modulating MS disease course. Chronotherapeutic approaches such as time-restricted eating (TRE) may benefit people with MS by stabilizing the circadian clock and restoring immunological and metabolic rhythms, thus potentially counteracting disease progression. This review provides a summary of selected studies on dietary intervention in MS, circadian rhythms, and their disruption in MS, including clock gene variations, circadian hormones, and retino-hypothalamic tract changes. Furthermore, we present studies that reported diurnal variations in MS, which might result from circadian disruption. And lastly, we suggest how chrononutritive approaches like TRE might counteract MS disease activity.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13939","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5805977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelets and endothelial dysfunction in gestational diabetes mellitus","authors":"Paola Valero,&nbsp;Marcelo Cornejo,&nbsp;Gonzalo Fuentes,&nbsp;Sergio Wehinger,&nbsp;Fernando Toledo,&nbsp;Eline M. van der Beek,&nbsp;Luis Sobrevia,&nbsp;Rodrigo Moore-Carrasco","doi":"10.1111/apha.13940","DOIUrl":"https://doi.org/10.1111/apha.13940","url":null,"abstract":"<p>The prevalence of gestational diabetes mellitus (GDM) has increased in recent years, along with the higher prevalence of obesity in women of reproductive age. GDM is a pathology associated with vascular dysfunction in the fetoplacental unit. GDM-associated endothelial dysfunction alters the transfer of nutrients to the foetus affecting newborns and pregnant women. Various mechanisms for this vascular dysfunction have been proposed, of which the most studied are metabolic alterations of the vascular endothelium. However, different cell types are involved in GDM-associated endothelial dysfunction, including platelets. Platelets are small, enucleated cell fragments that actively take part in blood haemostasis and thrombus formation. Thus, they play crucial roles in pathologies coursing with endothelial dysfunction, such as atherosclerosis, cardiovascular diseases, and diabetes mellitus. Nevertheless, platelet function in GDM is understudied. Several reports show a potential relationship between platelet volume and mass with GDM; however, platelet roles and signaling mechanisms in GDM-associated endothelial dysfunction are unclear. This review summarizes the reported findings and proposes a link among altered amount, volume, mass, reactivity, and function of platelets and placenta development, resulting in fetoplacental vascular dysfunction in GDM.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5833516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fifty years on: How we uncovered the unique bioenergetics of brown adipose tissue","authors":"David G. Nicholls","doi":"10.1111/apha.13938","DOIUrl":"https://doi.org/10.1111/apha.13938","url":null,"abstract":"<p>Exactly 50 years ago, I was a post-doc in the laboratory of Olov Lindberg in Stockholm measuring fatty acid oxidation by mitochondria isolated from thermogenic brown adipose tissue, when we noticed a curious nonlinearity in the respiration rate. This initiated a convoluted chain of experiments revealing that the mitochondria were textbook demonstrations of the then novel and highly controversial “chemiosmotic hypothesis” of Peter Mitchell and that thermogenesis was regulated by a proton short-circuit, mediated by a 32 kDa “uncoupling protein,” UCP1, activated by fatty acid. This review is a personal account of the research into the bioenergetics of isolated brown adipocytes and isolated mitochondria, which led, after fifteen years of investigation, to what is still accepted as the “canonical” UCP1-mediated mechanism of nonshivering thermogenesis, uniting whole animal physiology with mitochondrial bioenergetics.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5778653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rats lacking Ucp1 present a novel translational tool for the investigation of thermogenic adaptation during cold challenge","authors":"Jaycob D. Warfel,&nbsp;Carrie M. Elks,&nbsp;David S. Bayless,&nbsp;Bolormaa Vandanmagsar,&nbsp;Allison C. Stone,&nbsp;Samuel E. Velasquez,&nbsp;Paola Olivares-Nazar,&nbsp;Robert C. Noland,&nbsp;Sujoy Ghosh,&nbsp;Jingying Zhang,&nbsp;Randall L. Mynatt","doi":"10.1111/apha.13935","DOIUrl":"https://doi.org/10.1111/apha.13935","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Valuable studies have tested the role of UCP1 on body temperature maintenance in mice, and we sought to knockout <i>Ucp1</i> in rats (<i>Ucp1</i>^−/−) to provide insight into thermogenic mechanisms in larger mammals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used CRISPR/Cas9 technology to create <i>Ucp1</i>^−/− rats. Body weight and adiposity were measured, and rats were subjected to indirect calorimetry. Rats were maintained at room temperature or exposed to 4°C for either 24 h or 14 days. Analyses of brown and white adipose tissue and skeletal muscle were conducted via histology, western blot comparison of oxidative phosphorylation proteins, and qPCR to compare mitochondrial DNA levels and mRNA expression profiles. RNA-seq was performed in skeletal muscle.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p><i>Ucp1</i>^−/− rats withstood 4°C for 14 days, but core temperature steadily declined. All rats lost body weight after 14 days at 4°C, but controls increased food intake more robustly than <i>Ucp1</i>^−/− rats. Brown adipose tissue showed signs of decreased activity in <i>Ucp</i>1^−/− rats, while mitochondrial lipid metabolism markers in white adipose tissue and skeletal muscle were increased. <i>Ucp1</i>^−/− rats displayed more visible shivering and energy expenditure than controls at 4°C. Skeletal muscle transcriptomics showed more differences between genotypes at 23°C than at 4°C.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Room temperature presented sufficient cold stress to rats lacking UCP1 to activate compensatory thermogenic mechanisms in skeletal muscle, which were only activated in control rats following exposure to 4°C. These results provide novel insight into thermogenic responses to UCP1 deficiency; and highlight <i>Ucp</i>1^−/− rats as an attractive translational model for the study of thermogenesis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5699452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic effects of L-citrulline in type 2 diabetes","authors":"Fatemeh Bagheripour,&nbsp;Sajad Jeddi,&nbsp;Khosrow Kashfi,&nbsp;Asghar Ghasemi","doi":"10.1111/apha.13937","DOIUrl":"https://doi.org/10.1111/apha.13937","url":null,"abstract":"<p>The prevalence of type 2 diabetes (T2D) is increasing worldwide. Decreased nitric oxide (NO) bioavailability is involved in the pathophysiology of T2D and its complications. <span>L</span>-citrulline (Cit), a precursor of NO production, has been suggested as a novel therapeutic agent for T2D. Available data from human and animal studies indicate that Cit supplementation in T2D increases circulating levels of Cit and <span>L</span>-arginine while decreasing circulating glucose and free fatty acids and improving dyslipidemia. The underlying mechanisms for these beneficial effects of Cit include increased insulin secretion from the pancreatic β cells, increased glucose uptake by the skeletal muscle, as well as increased lipolysis and β-oxidation, and decreased glyceroneogenesis in the adipose tissue. Thus, Cit has antihyperglycemic, antidyslipidemic, and antioxidant effects and has the potential to be used as a new therapeutic agent in the management of T2D. This review summarizes available literature from human and animal studies to explore the effects of Cit on metabolic parameters in T2D. It also discusses the possible mechanisms underlying Cit-induced improved metabolic parameters in T2D.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"237 3","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5684085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}