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1.
Proc Natl Acad Sci U S A ; 121(12): e2306389121, 2024 Mar 19.
Artículo en Inglés | MEDLINE | ID: mdl-38437530

RESUMEN

How animals refine migratory behavior over their lifetime (i.e., the ontogeny of migration) is an enduring question with important implications for predicting the adaptive capacity of migrants in a changing world. Yet, our inability to monitor the movements of individuals from early life onward has limited our understanding of the ontogeny of migration. The exploration-refinement hypothesis posits that learning shapes the ontogeny of migration in long-lived species, resulting in greater exploratory behavior early in life followed by more rapid and direct movement during later life. We test the exploration-refinement hypothesis by examining how white storks (Ciconia ciconia) balance energy, time, and information as they develop and refine migratory behavior during the first years of life. Here, we show that young birds reduce energy expenditure during flight while also increasing information gain by exploring new places during migration. As the birds age and gain more experience, older individuals stop exploring new places and instead move more quickly and directly, resulting in greater energy expenditure during migratory flight. During spring migration, individuals innovated novel shortcuts during the transition from early life into adulthood, suggesting a reliance on spatial memory acquired through learning. These incremental refinements in migratory behavior provide support for the importance of individual learning within a lifetime in the ontogeny of long-distance migration.


Asunto(s)
Metabolismo Energético , Conducta Exploratoria , Humanos , Animales , Movimiento , Estaciones del Año , Memoria Espacial
2.
Diabetes Obes Metab ; 26 Suppl 2: 34-45, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38450938

RESUMEN

Hypothalamic obesity (HO) is a rare and complex disorder that confers substantial morbidity and excess mortality. HO is a unique subtype of obesity characterized by impairment in the key brain pathways that regulate energy intake and expenditure, autonomic nervous system function, and peripheral hormonal signalling. HO often occurs in the context of hypothalamic syndrome, a constellation of symptoms that follow from disruption of hypothalamic functions, for example, temperature regulation, sleep-wake circadian control, and energy balance. Genetic forms of HO, including the monogenic obesity syndromes, often impact central leptin-melanocortin pathways. Acquired forms of HO occur as a result of tumours impacting the hypothalamus, such as craniopharyngioma, surgery or radiation to treat those tumours, or other forms of hypothalamic damage, such as brain injury impacting the region. Risk for severe obesity following hypothalamic injury is increased with larger extent of hypothalamic damage or lesions that contain the medial and posterior hypothalamic nuclei that support melanocortin signalling pathways. Structural damage in these hypothalamic nuclei often leads to hyperphagia, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue, the collective effect of which is rapid weight gain. Individuals with hyperphagia are perpetually hungry. They do not experience fullness at the end of a meal, nor do they feel satiated after meals, leading them to consume larger and more frequent meals. To date, most efforts to treat HO have been disappointing and met with limited, if any, long-term success. However, new treatments based on the distinct pathophysiology of disturbed energy homeostasis in acquired HO may hold promise for the future.


Asunto(s)
Craneofaringioma , Enfermedades Hipotalámicas , Neoplasias Hipofisarias , Humanos , Leptina/metabolismo , Enfermedades Hipotalámicas/complicaciones , Enfermedades Hipotalámicas/terapia , Enfermedades Hipotalámicas/metabolismo , Obesidad/complicaciones , Obesidad/terapia , Obesidad/genética , Hipotálamo/metabolismo , Craneofaringioma/complicaciones , Craneofaringioma/terapia , Craneofaringioma/metabolismo , Hiperfagia , Neoplasias Hipofisarias/metabolismo , Neoplasias Hipofisarias/patología , Melanocortinas/metabolismo , Metabolismo Energético/fisiología
3.
J Exp Clin Cancer Res ; 43(1): 74, 2024 Mar 08.
Artículo en Inglés | MEDLINE | ID: mdl-38459595

RESUMEN

Glutamine metabolism plays a pivotal role in cancer progression, immune cell function, and the modulation of the tumor microenvironment. Dysregulated glutamine metabolism has been implicated in cancer development and immune responses, supported by mounting evidence. Cancer cells heavily rely on glutamine as a critical nutrient for survival and proliferation, while immune cells require glutamine for activation and proliferation during immune reactions. This metabolic competition creates a dynamic tug-of-war between cancer and immune cells. Targeting glutamine transporters and downstream enzymes involved in glutamine metabolism holds significant promise in enhancing anti-tumor immunity. A comprehensive understanding of the intricate molecular mechanisms underlying this interplay is crucial for developing innovative therapeutic approaches that improve anti-tumor immunity and patient outcomes. In this review, we provide a comprehensive overview of recent advances in unraveling the tug-of-war of glutamine metabolism between cancer and immune cells and explore potential applications of basic science discoveries in the clinical setting. Further investigations into the regulation of glutamine metabolism in cancer and immune cells are expected to yield valuable insights, paving the way for future therapeutic interventions.


Asunto(s)
Glutamina , Neoplasias , Humanos , Glutamina/metabolismo , Neoplasias/patología , Metabolismo Energético , Microambiente Tumoral
4.
Physiol Plant ; 176(2): e14262, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38522857

RESUMEN

Soybean (Glycine max) is economically significant, but the mechanisms underlying its adaptation to simultaneous low phosphorus and salt stresses are unclear. We employed the Shennong 94-1-8 soybean germplasm to conduct a comprehensive analysis, integrating both physiochemical and transcriptomic approaches, to unravel the response mechanisms of soybean when subjected to simultaneous low phosphorus and salt stresses. Remarkably, the combined stress exhibited the most pronounced impact on the soybean root system, which led to a substantial reduction in total soluble sugar (TSS) and total soluble protein (TSP) within the plants under this treatment. A total of 20,953 differentially expressed genes were identified through pairwise comparisons. Heatmap analysis of genes related to energy metabolism pathways demonstrated a significant down-regulation in expression under salt and low phosphorus + salt treatments, while low phosphorus treatment did not exhibit similar expression trends. Furthermore, the weighted gene co-expression network analysis (WGCNA) indicated that the blue module had a strong positive correlation with TSS and TSP. Notably, 2,3-bisphosphoglycerate-dependent phosphoglycerate mutase 1, FCS-Like Zinc finger 8, auxin response factor 18 isoform X2, and NADP-dependent malic enzyme emerged as hub genes associated with energy metabolism. In summary, our findings indicate that soybean roots are more adversely affected by salt and combined stress than by low phosphorus alone due to reduced activity in energy metabolism-related pathways and hub genes. These results offer novel insights into the adaptive mechanisms of soybeans when facing the combined stress of low phosphorus and salinity.


Asunto(s)
Estrés Fisiológico , /genética , Estrés Fisiológico/genética , Cloruro de Sodio/farmacología , Cloruro de Sodio/metabolismo , Perfilación de la Expresión Génica , Metabolismo Energético/genética , Fósforo/metabolismo , Regulación de la Expresión Génica de las Plantas
5.
Neurol India ; 72(1): 78-82, 2024 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-38443006

RESUMEN

BACKGROUND: In traumatic brain injuries (TBI), cerebral microdialysis (CMD)-derived parameters, especially the lactate to pyruvate ratio (LP ratio), have been utilized for cerebral perfusion optimization. The objectives were to identify cerebral ischemia as measured by CMD in TBI patients requiring decompressive craniectomy and to observe the correlation between cerebral perfusion pressure (CPP), intracranial pressure (ICP), and CMD variables in these patients. Our secondary aim was to observe the effect of CPP augmentation on ischemia biomarkers. METHODS: After the Institute Ethics Committee approvals, seven adult patients requiring decompressive craniectomy following TBI were enrolled and CMD data were obtained prospectively for 72 h. CPP was augmented by 20% with noradrenaline infusion if LP ratio >40. Correlations were done with bootstrapping (n = 500) to obtain the confidence intervals (CI) due to the small sample size. RESULTS: One patient had cerebral ischemia (median LP ratio of 265.5 and median pyruvate of 38 µmol/L), while another patient had non-ischemic mitochondrial dysfunction (median LP ratio 40.7 and median pyruvate 278.5). The coefficients of correlation between the LP ratio with CPP and ICP were r = -0.05 (CI = -0.14-0.03) and r = 0.09 (CI = -0.03-0.24), respectively. The coefficient of correlation between cerebral and blood glucose was r = 0.38, (CI - 0.35-0.14). Only two patients needed CPP augmentation, however, postaugmentation cerebral biochemistry did not change appreciably. CONCLUSION: CMD can identify cerebral ischemia, however, no correlations were observed between the LP ratio and CPP or ICP. CPP augmentation did not improve cerebral biochemistry. More studies are required to understand and treat cerebral metabolism in TBI.


Asunto(s)
Lesiones Traumáticas del Encéfalo , Encéfalo , Adulto , Humanos , Microdiálisis , Lesiones Traumáticas del Encéfalo/cirugía , Infarto Cerebral , Metabolismo Energético , Piruvatos
6.
Sheng Li Xue Bao ; 76(1): 161-172, 2024 Feb 25.
Artículo en Chino | MEDLINE | ID: mdl-38444141

RESUMEN

Mitophagy is a process that selectively removes excess or damaged mitochondria and plays an important role in regulating intracellular mitochondrial mass and maintaining mitochondrial energy metabolism. TANK-binding kinase 1 (TBK1) is a multifunctional serine/threonine protein kinase, which is involved in the regulation of PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent and -independent mitophagy. Recent studies have shown that TBK1 phosphorylates the autophagy related proteins, such as optineurin (OPTN), p62/sequestosome-1, Ras-related GTP binding protein 7 (Rab7), and mediates the binding of nuclear dot protein 52 (NDP52) to UNC-51 like autophagy activating kinase 1 (ULK1) complex, as well as the binding of TAX1-binding protein 1 (TAX1BP1) to microtubule-associated protein 1 light chain 3 (LC3), thereby enhancing PINK1/Parkin-dependent mitophagy. In addition, TBK1 is a direct substrate of AMP-activated protein kinase (AMPK)/ULK1 pathway, and its activation phosphorylates dynamin-related protein 1 (Drp1) and Rab7 to promote PINK1/Parkin-independent mitophagy. This article reviews the role and mechanism of TBK1 in regulating PINK1/Parkin-dependent and -independent mitophagy.


Asunto(s)
Mitofagia , Ubiquitina-Proteína Ligasas , Proteínas Quinasas Activadas por AMP , Autofagia , Metabolismo Energético
7.
Skin Res Technol ; 30(3): e13638, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38454567

RESUMEN

BACKGROUND: Skin wound healing is a complex mechanism which requires a lot of energy, mainly provided by mitochondrial respiration. However, little is known about the mitochondrial bioenergetics of mice skin. We sought to develop a microplate-based assay to directly measure oxygen consumption in whole mice skin with the goal of identifying mitochondrial dysfunction in diabetic skin using an extracellular flux. MATERIALS AND METHODS: Different parameters were optimized to efficiently measure the oxygen consumption rate (OCR). First, the most pertinent skin side of wild-type mice was first determined. Then, concentrations of mitochondrial inhibitors were then optimized to get the best efficacy. Finally, punch sizes were modulated to get the best OCR profile. RESULTS: Dermis had the best metabolic activity side of the skin. Unlike the increased concentrations of carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) and rotenone/antimycin A, which showed no improvement of these drugs' effects, varying the skin punch size was successful. Finally, type II diabetic (T2D) skin produced less ATP through mitochondrial metabolism and had a greater non-mitochondrial oxygen consumption than wild-type or type I diabetic (T1D) skin. CONCLUSION: Here we designed, for the first time, a reliable protocol to measure mitochondria function in whole mouse skin. Our optimized protocol was valuable in assessing alterations associated with diabetes and could be applied to future studies of pathological human skin metabolism.


Asunto(s)
Diabetes Mellitus Experimental , Ratones , Humanos , Animales , Diabetes Mellitus Experimental/inducido químicamente , Diabetes Mellitus Experimental/metabolismo , Mitocondrias/metabolismo , Metabolismo Energético , Consumo de Oxígeno , Carbonil Cianuro p-Trifluorometoxifenil Hidrazona/metabolismo , Carbonil Cianuro p-Trifluorometoxifenil Hidrazona/farmacología
9.
J Transl Med ; 22(1): 240, 2024 Mar 05.
Artículo en Inglés | MEDLINE | ID: mdl-38443933

RESUMEN

BACKGROUND: Mitochondria produce adenosine triphosphate through respiratory activities to power sperm differentiation and motility, and decreased mitochondrial respiratory activity can result in poor sperm motility and asthenospermia. The mitochondrial sheath is a component of the mid-piece of the sperm flagellum, and dysfunction of the sheath can reduce sperm motility and cause male infertility. The membrane occupation and recognition nexus-motif protein 2 (MORN2) is testis enriched in mice, and the MORN motif was reported to play a role in the regulation of bioelectrical signal homeostasis in cardiomyocytes. METHODS: We generated Morn2-/- mice using CRISPR/Cas9 and evaluated the potential functions of MORN2 in spermiogenesis through histological analysis, fertility examination, RT-PCR, CASA, immunofluorescence, TUNEL, electron microscopy analysis, mitochondrial energy metabolism analysis, etc. RESULTS: The Morn2-/- mice were infertile, and their sperm showed severe motility defects. Morn2-/- sperm also had abnormal morphology characterized by bent heads, aberrant mitochondrial sheath formation, lower mitochondrial membrane potential, higher levels of reactive oxygen species, and decreased mitochondrial respiratory activity. CONCLUSIONS: Our study demonstrates that MORN2 is essential for male fertility and indicates that MORN2 functions in mitochondrial sheath formation and regulates mitochondrial respiratory activity.


Asunto(s)
Semen , Motilidad Espermática , Animales , Masculino , Ratones , Metabolismo Energético , Fertilidad , Mitocondrias
10.
Curr Opin Crit Care ; 30(2): 186-192, 2024 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-38441116

RESUMEN

PURPOSE OF REVIEW: Recent changes in guidelines recommendation during early phase of critical illness and use of indirect calorimetry. The aim of this review is to discuss methods of determining energy requirements in the critically ill and highlight factors impacting resting energy expenditure. RECENT FINDING: An appraisal of recent literature discussing indirect calorimetry guided-nutrition potential benefits or pitfalls. Recent attempts to devise strategy and pilot indirect calorimetry use in the critically ill patients requiring continuous renal replacement therapy or extracorporeal membrane oxygenation are also discussed. Additionally, we briefly touched on variability between guidelines recommended energy target and measured energy expenditure for adult critically ill patients with obesity. SUMMARY: While energy requirement in the critically ill continues to be an area of controversy, recent guidelines recommendations shift toward providing less aggressive calories during acute phase of illness in the first week of ICU.Use of indirect calorimetry may provide more accurate energy target compared to the use of predictive equations. Despite the absence of literature to support long term mortality benefits, there are many potential benefits for the use of indirect calorimetry when available.


Asunto(s)
Enfermedad Crítica , Metabolismo Energético , Adulto , Humanos , Enfermedad Crítica/terapia , Calorimetría Indirecta/métodos , Obesidad , Ingestión de Energía
11.
Sci Rep ; 14(1): 6348, 2024 03 15.
Artículo en Inglés | MEDLINE | ID: mdl-38491051

RESUMEN

Hepatocellular carcinoma (HCC) progression is associated with dysfunctional mitochondria and bioenergetics impairment. However, no data about the relationship between mitochondrial supercomplexes (hmwSC) formation and ATP production rates in HCC are available. Our group has developed an adenosine derivative, IFC-305, which improves mitochondrial function, and it has been proposed as a therapeutic candidate for HCC. We aimed to determine the role of IFC-305 on both mitochondrial structure and bioenergetics in a sequential cirrhosis-HCC model in rats. Our results showed that IFC-305 administration decreased the number and size of liver tumors, reduced the expression of tumoral markers, and reestablished the typical architecture of the hepatic parenchyma. The livers of treated rats showed a reduction of mitochondria number, recovery of the mtDNA/nDNA ratio, and mitochondrial length. Also, IFC-305 increased cardiolipin and phosphatidylcholine levels and promoted hmwSC reorganization with changes in the expression levels of hmwSC assembly-related genes. IFC-305 in HCC modified the expression of several genes encoding elements of electron transport chain complexes and increased the ATP levels by recovering the complex I, III, and V activity. We propose that IFC-305 restores the mitochondrial bioenergetics in HCC by normalizing the quantity, morphology, and function of mitochondria, possibly as part of its hepatic restorative effect.


Asunto(s)
Carcinoma Hepatocelular , Neoplasias Hepáticas , Ratas , Animales , Carcinoma Hepatocelular/inducido químicamente , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/metabolismo , Dietilnitrosamina/toxicidad , Neoplasias Hepáticas/inducido químicamente , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , Mitocondrias/metabolismo , Adenosina/metabolismo , Metabolismo Energético , Adenosina Trifosfato/metabolismo
12.
ACS Appl Bio Mater ; 7(3): 1862-1877, 2024 Mar 18.
Artículo en Inglés | MEDLINE | ID: mdl-38450575

RESUMEN

Elevated levels of reactive oxygen species (ROS) have demonstrated efficacy in eliminating tumor cells by modifying the tumor microenvironment and inducing the polarization of tumor-associated macrophages (TAMs). Nevertheless, the transient nature and limited diffusion distance inherent in ROS present significant challenges in cancer treatment. In response to these limitations, we have developed a nanoparticle (MnClPc-HSA@GOx) that not only inhibits tumor energy metabolism but also facilitates the transition of TAMs from the M2 type (anti-inflammatory type) to the M1 type (proinflammatory type). MnClPc-HSA@GOx comprises a manganese phthalocyanine complex (MnClPc) enveloped in human serum albumin (HSA), with glucose oxidase (GOx) loaded onto MnClPc@HSA nanoparticles. GOx was employed to catalyze the decomposition of glucose to produce H2O2 and gluconic acid. Additionally, in the presence of MnClPc, it catalyzes the conversion of H2O2 into •O2- and 1O2. Results indicate that the nanoparticle effectively impedes the glucose supply to tumor cells and suppresses their energy metabolism. Simultaneously, the ROS-mediated polarization of TAMs induces a shift from M2 to M1 macrophages, resulting in a potent inhibitory effect on tumors. This dual-action strategy holds promising clinical inhibition applications in the treatment of cancer.


Asunto(s)
Isoindoles , Nanopartículas , Neoplasias , Humanos , Manganeso/farmacología , Glucosa Oxidasa/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Peróxido de Hidrógeno/metabolismo , Neoplasias/metabolismo , Macrófagos , Oxígeno/metabolismo , Metabolismo Energético , Glucosa , Microambiente Tumoral
13.
Cardiovasc Diabetol ; 23(1): 96, 2024 Mar 14.
Artículo en Inglés | MEDLINE | ID: mdl-38486199

RESUMEN

Diabetic cardiomyopathy (DCM) is a major contributor to mortality in diabetic patients, characterized by a multifaceted pathogenesis and limited therapeutic options. While lactate, a byproduct of glycolysis, is known to be significantly elevated in type 2 diabetes, its specific role in DCM remains uncertain. This study reveals an abnormal upregulation of monocarboxylate transporter 4 (MCT4) on the plasma membrane of cardiomyocytes in type 2 diabetes, leading to excessive lactate efflux from these cells. The disruption in lactate transport homeostasis perturbs the intracellular lactate-pyruvate balance in cardiomyocytes, resulting in oxidative stress and inflammatory responses that exacerbate myocardial damage. Additionally, our findings suggest increased lactate efflux augments histone H4K12 lactylation in macrophages, facilitating inflammatory infiltration within the microenvironment. In vivo experiments have demonstrated that inhibiting MCT4 effectively alleviates myocardial oxidative stress and pathological damage, reduces inflammatory macrophage infiltration, and enhances cardiac function in type 2 diabetic mice. Furthermore, a clinical prediction model has been established, demonstrating a notable association between peripheral blood lactate levels and diastolic dysfunction in individuals with type 2 diabetes. This underscores the potential of lactate as a prognostic biomarker for DCM. Ultimately, our findings highlight the pivotal involvement of MCT4 in the dysregulation of cardiac energy metabolism and macrophage-mediated inflammation in type 2 diabetes. These insights offer novel perspectives on the pathogenesis of DCM and pave the way for the development of targeted therapeutic strategies against this debilitating condition.


Asunto(s)
Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 2 , Cardiomiopatías Diabéticas , Animales , Humanos , Ratones , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Cardiomiopatías Diabéticas/etiología , Metabolismo Energético , Inflamación , Ácido Láctico/metabolismo , Modelos Estadísticos , Pronóstico
14.
Aging (Albany NY) ; 16(5): 4469-4502, 2024 Mar 04.
Artículo en Inglés | MEDLINE | ID: mdl-38441550

RESUMEN

BACKGROUND: Prostate cancer is the most common malignancy among men worldwide, and its diagnosis and treatment are challenging due to its heterogeneity. METHODS: Integrating single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data, we identified two molecular subtypes of prostate cancer based on dysregulated genes involved in oxidative stress and energy metabolism. We constructed a risk score model (OMR) using common differentially expressed genes, which effectively evaluated prostate cancer prognosis. RESULTS: Our analysis demonstrated a significant correlation between the risk score model and various factors, including tumor immune microenvironment, genomic variations, chemotherapy resistance, and immune response. Notably, patients with low-risk scores exhibited increased sensitivity to chemotherapy and immunotherapy compared to those with high-risk scores, indicating the model's potential to predict patient response to treatment. Additionally, our investigation of MXRA8 in prostate cancer showed significant upregulation of this gene in the disease as confirmed by PCR and immunohistochemistry. Functional assays including CCK-8, transwell, plate cloning, and ROS generation assay demonstrated that depletion of MXRA8 reduced the proliferative, invasive, migratory capabilities of PC-3 cells, as well as their ROS generation capacity. CONCLUSIONS: Our study highlights the potential of oxidative stress and energy metabolism-related genes as prognostic markers and therapeutic targets in prostate cancer. The integration of scRNA-seq and bulk RNA-seq data enables a better understanding of prostate cancer heterogeneity and promotes personalized treatment development. Additionally, we identified a novel oncogene MXRA8 in prostate cancer.


Asunto(s)
Oncogenes , Neoplasias de la Próstata , Humanos , Masculino , Metabolismo Energético/genética , Estrés Oxidativo/genética , Pronóstico , Neoplasias de la Próstata/genética , Especies Reactivas de Oxígeno , Microambiente Tumoral/genética , Proteínas de la Membrana/genética , Inmunoglobulinas/genética
15.
J Strength Cond Res ; 38(4): 755-761, 2024 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-38513180

RESUMEN

ABSTRACT: Pilon, R, Matos-Santos, L, Matlez, MP, Rodrigues, G, Amorim, F, Lattari, E, Farinatti, P, and Monteiro, W. Effects of isocaloric resistance, aerobic, and concurrent exercise on excess postexercise oxygen consumption in older adults. J Strength Cond Res 38(4): 755-761, 2024-Excess postexercise oxygen consumption (EPOC) is a major determinant of exercise-related caloric expenditure and metabolic adaptations. Exercise modality may influence the EPOC, but this issue has not been investigated in older adults. This study compared the EPOC after isocaloric bouts of continuous aerobic exercise (AE), resistance exercise (RE), and concurrent exercise (CE) in older individuals. Ten subjects (5 men; 73 ± 6 years) had their cardiorespiratory data assessed during AE, RE, and CE and along 30-minute postexercise recovery. Total energy expenditure (EE) during exercise was similar (p > 0.05) in AE (126.0 ± 30.7 kcal), RE (123.9 ± 30.6 kcal), and CE (130.8 ± 32.6 kcal), with different times to achieve the targeted EE (RE: 61.4 ± 1.9 minutes > CE: 43.3 ± 5.6 minutes > AE: 26.6 ± 5.7 minutes; p < 0.001). Consistently, the relative intensity during exercise was superior (p < 0.05) in AE (74 ± 15% oxygen uptake reserve [VO2R]) vs. CE (43 ± 13% VO2R) vs. RE (24 ± 9% VO2R). Despite the isocaloric conditions, average EPOC and EE were approximately 45% greater (p < 0.001) in AE (8.0 ± 2.3 L; 40.1 ± 11.7 kcal) vs. RE (5.6 ± 1.2 L; 28.1 ± 5.8 kcal) and CE (5.4 ± 2.3 L; 26.9 ± 11.5 kcal). In conclusion, the EPOC was greater after isocaloric AE vs. RE and CE performed by older adults. Exercise intensity seemed to be a more important determinant of EPOC than volume reflected by EE during exercise bouts. Moderate-intensity continuous AE was more time-efficient than RE and CE to achieve a target EE. In older individuals, AE should be preferred over RE or CE when the purpose is to increase the daily caloric expenditure.


Asunto(s)
Metabolismo Energético , Ejercicio Físico , Masculino , Humanos , Anciano , Pruebas de Función Respiratoria , Prueba de Esfuerzo , Consumo de Oxígeno
16.
Nat Commun ; 15(1): 2543, 2024 Mar 21.
Artículo en Inglés | MEDLINE | ID: mdl-38514654

RESUMEN

Accumulating evidence points to dysregulations of the Nucleus Accumbens (NAc) in eating disorders (ED), however its precise contribution to ED symptomatic dimensions remains unclear. Using chemogenetic manipulations in male mice, we found that activity of dopamine D1 receptor-expressing neurons of the NAc core subregion facilitated effort for a food reward as well as voluntary exercise, but decreased food intake, while D2-expressing neurons have opposite effects. These effects are congruent with D2-neurons being more active than D1-neurons during feeding while it is the opposite during running. Chronic manipulations of each subpopulations had limited effects on energy balance. However, repeated activation of D1-neurons combined with inhibition of D2-neurons biased behavior toward activity-related energy expenditure, whilst the opposite manipulations favored energy intake. Strikingly, concomitant activation of D1-neurons and inhibition of D2-neurons precipitated weight loss in anorexia models. These results suggest that dysregulations of NAc dopaminoceptive neurons might be at the core of EDs.


Asunto(s)
Núcleo Accumbens , Receptores de Dopamina D2 , Ratones , Masculino , Animales , Núcleo Accumbens/metabolismo , Receptores de Dopamina D2/genética , Receptores de Dopamina D2/metabolismo , Neuronas/metabolismo , Receptores de Dopamina D1/genética , Receptores de Dopamina D1/metabolismo , Metabolismo Energético
17.
J Biosci ; 492024.
Artículo en Inglés | MEDLINE | ID: mdl-38516912

RESUMEN

Phototrophic organisms harbor two main bioenergetic hubs, photosynthesis and respiration, and these processes dynamically exchange and share metabolites to balance the energy of the cell. In microalgae and cyanobacteria, the crosstalk between the light-triggered reactions of photosynthesis and respiration is particularly prominent with respiratory O2 uptake which can be stimulated upon illumination. Since its discovery, this light-enhanced respiration has been proposed to be critical in dissipating the excess reducing power generated by photosynthesis. Importantly, the physiological role and putative molecular mechanism involved have just recently started to be understood. Here, we revisit the physiological functions and discuss possible molecular mechanisms of interactions between the photosynthetic and respiratory electron flows in microalgae and cyanobacteria.


Asunto(s)
Cianobacterias , Fotosíntesis , Transporte de Electrón/genética , Fotosíntesis/genética , Metabolismo Energético , Respiración , Cianobacterias/genética
18.
Int J Oncol ; 64(4)2024 04.
Artículo en Inglés | MEDLINE | ID: mdl-38426621

RESUMEN

Tumor malignant cells are characterized by dysregulation of mitochondrial bioenergetics due to the 'Warburg effect'. In the present study, this metabolic imbalance was explored as a potential target for novel cancer chemotherapy. Imatinib (IM) downregulates the expression levels of SCΟ2 and FRATAXIN (FXN) genes involved in the heme­dependent cytochrome c oxidase biosynthesis and assembly pathway in human erythroleukemic IM­sensitive K­562 chronic myeloid leukemia cells (K­562). In the present study, it was investigated whether the treatment of cancer cells with IM (an inhibitor of oxidative phosphorylation) separately, or together with dichloroacetate (DCA) (an inhibitor of glycolysis), can inhibit cell proliferation or cause death. Human K­562 and IM­chemoresistant K­562 chronic myeloid leukemia cells (K­562R), as well as human colorectal carcinoma cells HCT­116 (+/+p53) and (­/­p53, with double TP53 knock-in disruptions), were employed. Treatments of these cells with either IM (1 or 2 µM) and/or DCA (4 mΜ) were also assessed for the levels of several process biomarkers including SCO2, FXN, lactate dehydrogenase A, glyceraldehyde­3­phosphate dehydrogenase, pyruvate kinase M2, hypoxia inducing factor­1a, heme oxygenase­1, NF­κB, stem cell factor and vascular endothelial growth factor via western blot analysis. Computational network biology models were also applied to reveal the connections between the ten proteins examined. Combination treatment of IM with DCA caused extensive cell death (>75%) in K­562 and considerable (>45%) in HCT­116 (+/+p53) cultures, but less in K­562R and HCT­116 (­/­p53), with the latter deficient in full length p53 protein. Such treatment, markedly reduced reactive oxygen species levels, as measured by flow­cytometry, in K­562 cells and affected the oxidative phosphorylation and glycolytic biomarkers in all lines examined. These findings indicated, that targeting of cancer mitochondrial bioenergetics with such a combination treatment was very effective, although chemoresistance to IM in leukemia and the absence of a full length p53 in colorectal cells affected its impact.


Asunto(s)
Neoplasias Colorrectales , Leucemia Eritroblástica Aguda , Leucemia Mielógena Crónica BCR-ABL Positiva , Humanos , Mesilato de Imatinib/farmacología , Mesilato de Imatinib/uso terapéutico , Proteína p53 Supresora de Tumor/genética , Factor A de Crecimiento Endotelial Vascular/metabolismo , Apoptosis , Línea Celular Tumoral , Leucemia Mielógena Crónica BCR-ABL Positiva/tratamiento farmacológico , Leucemia Mielógena Crónica BCR-ABL Positiva/genética , Leucemia Mielógena Crónica BCR-ABL Positiva/patología , Metabolismo Energético , Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/genética , Biomarcadores/metabolismo , Células K562 , Resistencia a Antineoplásicos/genética , Proliferación Celular
19.
Elife ; 122024 Mar 11.
Artículo en Inglés | MEDLINE | ID: mdl-38466325

RESUMEN

Imidacloprid is a global health threat that severely poisons the economically and ecologically important honeybee pollinator, Apis mellifera. However, its effects on developing bee larvae remain largely unexplored. Our pilot study showed that imidacloprid causes developmental delay in bee larvae, but the underlying toxicological mechanisms remain incompletely understood. In this study, we exposed bee larvae to imidacloprid at environmentally relevant concentrations of 0.7, 1.2, 3.1, and 377 ppb. There was a marked dose-dependent delay in larval development, characterized by reductions in body mass, width, and growth index. However, imidacloprid did not affect on larval survival and food consumption. The primary toxicological effects induced by elevated concentrations of imidacloprid (377 ppb) included inhibition of neural transmission gene expression, induction of oxidative stress, gut structural damage, and apoptosis, inhibition of developmental regulatory hormones and genes, suppression of gene expression levels involved in proteolysis, amino acid transport, protein synthesis, carbohydrate catabolism, oxidative phosphorylation, and glycolysis energy production. In addition, we found that the larvae may use antioxidant defenses and P450 detoxification mechanisms to mitigate the effects of imidacloprid. Ultimately, this study provides the first evidence that environmentally exposed imidacloprid can affect the growth and development of bee larvae by disrupting molting regulation and limiting the metabolism and utilization of dietary nutrients and energy. These findings have broader implications for studies assessing pesticide hazards in other juvenile animals.


Asunto(s)
Metabolismo Energético , Muda , Neonicotinoides , Nitrocompuestos , Abejas , Animales , Larva , Proyectos Piloto , Nutrientes
20.
Front Endocrinol (Lausanne) ; 15: 1323093, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38476670

RESUMEN

Introduction: Exploring the energy expenditure and substrate metabolism data during exercise, 10-minute recovery, and 20-minute recovery phases in Tabata, HIIT(High-Intensity Interval Training), and MICT(Moderate-Intensity Continuous Training). This study explores the scientific aspects of weight reduction strategies, examining energy expenditure and substrate metabolism from various training perspectives. The aim is to establish a theoretical foundation for tailoring targeted exercise plans for individuals within the population with overweight/obesity. Methods: This study used an experimental design with fifteen male university students with overweight/obesity. Participants underwent random testing with Tabata, HIIT, and MICT. Tabata involved eight sets of 20 seconds exercise and 10 seconds rest, totaling 4 minutes. HIIT included four sets of power cycling: 3 minutes at 80% VO2max intensity followed by 2 minutes at 20% VO2max. MICT comprised 30 minutes of exercise at 50% VO2max intensity. Gas metabolism indices were continuously measured. Subsequently, fat and glucose oxidation rates, along with energy expenditure, were calculated for each exercise type. Results: During both the exercise and recovery phases, the Tabata group exhibited a significantly higher fat oxidation rate of (0.27 ± 0.03 g/min) compared to the HIIT group (0.20 ± 0.04 g/min, p<0.05) and the MICT group (0.20 ± 0.03g/min, p<0.001). No significant difference was observed between the HIIT and MICT groups (p=0.854). In terms of energy expenditure rate, the Tabata group maintained a substantially elevated level at 5.76 ± 0.74kcal/min compared to the HIIT group (4.81 ± 0.25kcal/min, p<0.01) and the MICT group (3.45 ± 0.25kcal/min, p<0.001). Additionally, the energy expenditure rate of the HIIT group surpassed that of the MICT group significantly (p<0.001). Conclusion: The study finds that male college students with overweight/obesity in both exercise and recovery, Tabata group has lower fat and glucose oxidation rates, and energy expenditure compared to HIIT and MICT groups. However, over the entire process, Tabata still exhibits significantly higher rates in these aspects than HIIT and MICT. Despite a shorter exercise duration, Tabata shows a noticeable "time-efficiency" advantage. Tabata can be used as an efficient short-term weight loss exercise program for male college students with overweight/obesity.


Asunto(s)
Entrenamiento de Intervalos de Alta Intensidad , Sobrepeso , Humanos , Masculino , Sobrepeso/metabolismo , Universidades , Obesidad , Metabolismo Energético , Glucosa
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