Increasing dietary fiber intake for type 2 diabetes mellitus management: A systematic review.

BACKGROUND: Type 2 diabetes is a chronic, non-communicable disease with a substantial global impact, affecting a significant number of individuals. Its etiology is closely tied to imbalanced dietary practices and sedentary lifestyles. Conversely, increasing die-tary fiber (DF) intake has consistently demonstrated health benefits in numerous studies, including improvements in glycemic control and weight management. AIM: To investigate the efficacy of DF interventions in the management of type 2 diabetes mellitus (T2DM). METHODS: A systematic literature review was conducted to explore the association between DF intake and the management of T2DM. Following the inclusion and exclusion criteria, a total of 26 studies were included in this review. RESULTS: The main strategies implied to increased DF intake were: High DF diet plus acarbose (2 studies); DF supplements (14 studies); and high DF diets (10 studies). Overall, most studies indicated that increased DF intake resulted in im-provements in glycemic control and weight management in T2DM patients. CONCLUSION: DF represents a valuable strategy in the treatment of type 2 diabetes, improving health outcomes. DF intake offers the potential to improve quality of life and reduce complications and mortality associated with diabetes. Likewise, through supplements or enriched foods, DF contributes significantly to the control of several markers such as HbA1c, blood glucose, triglycerides, low-density lipoprotein, and body weight.

Shock index and its variants as predictors of mortality in severe traumatic brain injury.

BACKGROUND: The increase in severe traumatic brain injury (sTBI) incidence is a worldwide phenomenon, resulting in a heavy disease burden in the public health systems, specifically in emerging countries. The shock index (SI) is a physiological parameter that indicates cardiovascular status and has been used as a tool to assess the presence and severity of shock, which is increased in sTBI. Considering the high mortality of sTBI, scrutinizing the predictive potential of SI and its variants is vital. AIM: To describe the predictive potential of SI and its variants in sTBI. METHODS: This study included 71 patients (61 men and 10 women) divided into two groups: Survival (S; n = 49) and Non-survival (NS; n = 22). The responses of blood pressure and heart rate (HR) were collected at admission and 48 h after admission. The SI, reverse SI (rSI), rSI multiplied by the Glasgow Coma Score (rSIG), and Age multiplied SI (AgeSI) were calculated. Group comparisons included Shapiro-Wilk tests, and independent samples t-tests. For predictive analysis, logistic regression, receiver operator curves (ROC) curves, and area under the curve (AUC) measurements were performed. RESULTS: No significant differences between groups were identified for SI, rSI, or rSIG. The AgeSI was significantly higher in NS patients at 48 h following admission (S: 26.32 ± 14.2, and NS: 37.27 ± 17.8; P = 0.016). Both the logistic regression and the AUC following ROC curve analysis showed that only AgeSI at 48 h was capable of predicting sTBI outcomes. CONCLUSION: Although an altered balance between HR and blood pressure can provide insights into the adequacy of oxygen delivery to tissues and the overall cardiac function, only the AgeSI was a viable outcome-predictive tool in sTBI, warranting future research in different cohorts.

Role of the phase angle in the prognosis of the cirrhotic patient: 15 years of follow-up.

BACKGROUND: In 2019, cirrhosis accounted for 2.4% of global deaths. The projection for 2030 is an increase in this index. In recent years, hospitalization costs have escalated by 36% for compensated cirrhosis and 24% for decompensated cirrhosis. Therefore, it is necessary to identify a tool capable of predicting the mortality of these patients according to their clinical condition and consequently extending their survival time. Different studies have shown that the phase angle (PA) can be a feasible method in clinical practice, with the potential to guide assertive patient management in the therapeutic of chronic liver disease. AIM: To evaluate the prognostic role of PA in cirrhotic patients over a 15-year follow-up period. METHODS: Retrospective cohort study with 129 cirrhotic patients of both sexes over 18 years old. Diagnosis of cirrhosis by liver biopsy. The first year of data collection was 2007, and data regarding outcomes was collected in 2023. Data were gathered from medical records, such as esophageal varices (EV), EV bleeding, ascites, spontaneous bacterial peritonitis (SBP), encephalopathy, laboratory findings and PA. The cut-off value for the PA was 5.4°, a value described in 2012 by Fernandes et al for 129 patients evaluated in this study and the cut-off points for the Brazilian population presented in percentiles (P), as described by Mattiello et al. The mortality was assessed using the PA percentile through Kaplan-Meier curves and multivariate binary logistic regression models. RESULTS: Patients were divided into two groups according to the PA 5.4th (PA > 5.4°, n = 40; PA ≤ 5.4°, n = 89) PA percentile (< P50, n = 56; ≥ P50 n = 73). The percentile classification was more accurate in identifying long-term deaths than the 5.4º PA. Patients with < P50 had a higher number of relevant complications such as ascites, SBP, liver encephalopathy and HCC. PA is strongly correlated with serum albumin (P < 0.001), International Normalized Ratio (P = 0.01), total bilirubin (P = 0.02) and direct bilirubin (P = 0.003). PA is correlated with survival time (P < 0.001) and length of stay (P = 0.02). Logistic regression analysis shows that an increase of 1° in PA enlarges the cirrhotic patient's chance of survival by 17.7%. CONCLUSION: PA is a good predictor of morbidity and mortality for cirrhotic patients. The PA by percentile showed greater sensitivity in predicting mortality compared to the cut-off point of 5.4º.

Lower and higher volumes of physical exercise build up brain reserves against memory deficits triggered by a head injury in mice.

Decreasing neurotrophic support and impaired mitochondrial bioenergetics are key mechanisms for long-term neurodegeneration and cognitive decline after traumatic brain injury (TBI). We hypothesize that preconditioning with lower and higher volumes of physical exercise upregulates the CREB-BDNF axis and bioenergetic capability, which might serve as neural reserves against cognitive impairment after severe TBI. Using a running wheel mounted in the home cage, mice were engaged in lower (LV, 48 h free access, and 48 h locked) and higher (HV, daily free access) exercise volumes for thirty days. Subsequently, LV and HV mice remained for additional thirty days in the home cage with the running wheel locked and were euthanized. The sedentary group had the running wheel always locked. For the same type of exercise stimulus in a given time, daily workout presents higher volume than alternate days workout. The total distance ran in the wheel was the reference parameter to confirm distinct exercise volumes. On average, LV exercise ran 27.522 m and HV exercise ran 52.076 m. Primarily, we investigate whether LV and HV protocols increase neurotrophic and bioenergetic support in the hippocampus thirty days after exercise ceased. Regardless of volume, exercise increased hippocampal pCREBSer133-CREB-proBDNF-BDNF signaling and mitochondrial coupling efficiency, excess capacity, and leak control, that may compose the neurobiological basis for neural reserves. Further, we challenge these neural reserves against secondary memory deficits triggered by a severe TBI. After thirty days of exercise LV and HV, and sedentary (SED) mice were submitted to the CCI model. Mice remained for additional thirty days in the home cage with the running wheel locked. The mortality after severe TBI was approximately 20% in LV and HV, while in the SED was 40%. Also, LV and HV exercise sustained hippocampal pCREBSer133-CREB-proBDNF-BDNF signaling, mitochondrial coupling efficiency, excess capacity, and leak control for thirty days after severe TBI. Corroborating these benefits, the mitochondrial H2O2 production linked to complexes I and II was attenuated by exercise regardless of the volume. These adaptations attenuated spatial learning and memory deficits caused by TBI. In summary, preconditioning with LV and HV exercise builds up long-lasting CREB-BDNF and bioenergetic neural reserves that preserve memory fitness after severe TBI.

Relationship between phase angle, steatosis, and liver fibrosis in patients coinfected with human immunodeficiency virus/hepatitis C virus.

BACKGROUND: Malnutrition, lipodystrophy, and dyslipidemia are prevalent characteristics in patients with human immunodeficiency virus (HIV) infection with or without previous treatment. Such a clinical condition can lead to the hypothesis of the presence of hepatic steatosis with possible progression to fibrosis and the risk of hepatocellular carcinoma. Notably, a low phase angle (PA), evaluated by bioelectrical impedance analysis (BIA), is an independent prognostic marker of clinical progression and survival in HIV-infected patients. AIM: To evaluate the relationship between PA and body composition with steatosis and hepatic fibrosis in HIV/hepatitis C virus (HCV)-coinfected patients. METHODS: A retrospective observational study by convenience sampling of coinfected HIV/HCV patients, in which all patients underwent transient elastography (Fibroscan) and BIA evaluation. Student's t test was used for group comparisons, and Spearman's or Pearson's correlation test was used when appropriate. The significance level was set at 5%, and analyses were performed using SPSS version 21.0. RESULTS: Forty-three patients who received antiretroviral therapy met the inclusion criteria, and 23 (53.5%) were under treatment with protease inhibitors (PIs). There was no difference in PA between those who used PIs and those who did not (P = 0.635). There was no correlation between fibrosis grade and PA (P = 0.355) or lean mass (P = 0.378). There was a significant inverse correlation between the controlled attenuation parameter (CAP) and lean mass (P = 0.378), positive correlation between PA and lean mass (P = 0.378), and negative correlation between PA and fatty mass (P = 0.378), although the CAP and PA were not correlated. When evaluated by sex, no significant correlations were found. CONCLUSION: PA determines the muscle function of HIV/HCV-coinfected patients, and the CAP values reinforce the association with lean mass, suggesting that patients require early nutritional interventions.

Assessment of resting energy expenditure in patients with cirrhosis.

BACKGROUND: Malnutrition affects 20% to 50% of patients with cirrhosis. It may be associated with serious complications and has a direct impact on prognosis. Resting energy expenditure (REE) is an important parameter to guide the optimization of therapy and recovery of nutritional status in patients with cirrhosis. However, the REE of patients with cirrhosis is still unclear, casting doubt upon the optimal nutritional management approach. AIM: To identify the best method that predicts the REE of cirrhotic patients, using indirect calorimetry (IC) as the gold standard. METHODS: An observational study was performed on 90 patients with cirrhosis. REE was assessed by IC, bioelectrical impedance analysis (BIA), and predictive formulas, which were compared using Bland-Altman plots and the Student's t-test. RESULTS: REE values measured by IC (1607.72 ± 257.4 kcal) differed significantly from those determined by all other methods (BIA: 1790.48 ± 352.1 kcal; Harris & Benedict equation: 2373.54 ± 254.9 kcal; IOM equation: 1648.95 ± 185.6 kcal; Cunningham equation: 1764.29 ± 246.2 kcal), except the Food and Agriculture Organization of the United Nations, World Health Organization, and United Nations University (FAO/WHO/UNU) (1616.07 ± 214.6 kcal) and McArdle (1611.30 ± 241.8 kcal) equations. We found no significant association when comparing IC and 24-h dietary recall among different Child-Pugh classes of cirrhosis. CONCLUSION: The IOM and FAO/WHO/UNU equations have the best agreement with the CI. These results indicate a possibility of different tools for the clinical practice on cirrhotic patients.

A scoping review of intermittent fasting, chronobiology, and metabolism.

Chronobiology plays a crucial role in modulating many physiologic systems in which there is nutritional synergism with meal timing. Given that intermittent fasting (IF) has grown as a flexible dietary method consisting of delayed or early eating windows, this scoping review addresses the effects of IF protocols on metabolism as they relate to clinical nutrition and the circadian system. Although nocturnal habits are associated with circadian misalignments and impaired cardiometabolic profile-and nutritional physiology is better orchestrated during the day-most findings are based on animal experiments or human studies with observational designs or acute meal tests. Well-controlled randomized clinical trials employing IF protocols of delayed or early eating windows have sometimes demonstrated clinical benefits, such as improved glycemic and lipid profiles, as well as weight loss. However, IF does not appear to be more effective than traditional diets at the group level, and its effects largely depend on energy restriction. Thus, efforts must be made to identify patient biological rhythms, preferences, routines, and medical conditions before individual dietary prescription in clinical practice.

Anabolic-androgenic steroids impair mitochondrial function and redox status in the heart and liver of mice.

Supraphysiological doses of anabolic-androgenic steroids (AAS) may cause long-term functional abnormalities, particularly in the heart and liver, which may only represent the later-stage of the cumulative damage caused by dysfunctional organelles. We investigated whether mid-term supraphysiological doses of Testosterone and Nandrolone impair mitochondrial Ca2+ and membrane potential (ΔΨm) dynamics, and redox machinery in the heart and liver of mice. CF1 albino mice were treated daily with 15 mg/kg of Nandrolone (ND) or Testosterone (T), or oil (vehicle) for 19 days. Preparations enriched in mitochondria from the heart or liver were used to perform assays of Ca2+ influx/efflux, ΔΨm, and H2O2 production. ND significantly impaired mitochondrial Ca2+ influx in the heart, and ΔΨm in both organs. ND and T increased H2O2 levels in the heart and liver relative to controls. Also, ND increased oxidative damage to lipids and proteins (TBARS and carbonyls) in the heart, and both AAS decreased glutathione peroxidase activity in the heart and liver. In summary, supraphysiological doses of ND, and in a lesser extend T, impaired mitochondrial Ca2+ influx and ΔΨm, and redox homeostasis being early mechanistic substrates for inducing heart and liver tissue damage.

Intermittent fasting promotes anxiolytic-like effects unrelated to synaptic mitochondrial function and BDNF support.

Anxiety disorders are linked to mitochondrial dysfunction and decreased neurotrophic support. Since anxiolytic drugs target mitochondria, non-pharmacological approaches to improve mitochondrial metabolism such as intermittent fasting (IF) may cause parallel behavioral benefits against anxiety disorders. Here, we investigated whether a chronic IF regimen could induce anxiolytic-like effects concomitantly to modulation in mitochondrial bioenergetics and trophic signaling in mice brain. A total of 44 Male C57BL/6 J mice (180 days old) were assigned to two dietary regimens: a normal, ad libitum diet (AL group) and an alternate-day fasting (IF group), where animals underwent 10 cycles of 24 h food restriction followed by 24 h ad libitum access. Animals underwent the open field test, dark/light box and elevated plus maze tasks. Isolated nerve terminals were obtained from mice brain and used for mitochondrial respirometry, hydrogen peroxide production and assessment of membrane potential dynamics, calcium handling and western blotting. We showed that IF significantly alters total daily food intake and food consumption patterns but not body weight. There were no differences in the exploratory and locomotory parameters. Remarkably, animals from IF showed decreased anxiety-like behavior. Mitochondrial metabolic responses in different coupling states and parameters linked with H2O2 production, Ca2+ buffering and electric gradient were not different between groups. Finally, no alterations in molecular indicators of apoptotic death (Bax/Bcl-2 ratio) and neuroplasticity (proBDNF/BDNF and synaptophysin were observed). In conclusion, IF exerts anxiolytic-like effect not associated with modulation in synaptic neuronergetics or expression of neurotrophic proteins. These results highlight a potential benefit of intermittent fasting as a nutritional intervention in anxiety-related disorders.

Glutamate transporter-1 link astrocytes with heightened aggressive behavior induced by steroid abuse in male CF1 mice.

The astrocytic glutamate transporter GLT-1 performs glutamate uptake thereby mediating NMDAr responses in neurons. Ceftriaxone (CEF) upregulates astrocytic GLT-1 expression/activity, which could counteract excessive glutamate levels and aggressive behavior induced by anabolic synthetic steroids such as nandrolone decanoate (ND). Here, adult male CF-1 mice were allocated to oil (VEH), ND, CEF, and ND/CEF groups. Mice were subcutaneously (s.c.) injected with ND (15 mg/kg) or VEH for 19 days, and received intraperitoneal (i.p.) injections of CEF (200 mg/kg) or saline for 5 days. The ND/CEF group received ND for 19 days plus coadministration of CEF in the last 5 days. On the 19th day, the aggressive phenotypes were evaluated through the resident-intruder test. After 24 h, cerebrospinal fluid was collected to measure glutamate levels, and the pre-frontal cortex was used to assess GLT-1, pGluN2BTyr1472, and pGluN2ATyr1246 by Western blot. Synaptosomes from the left brain hemisphere was used to evaluate mitochondrial function including complex II-succinate dehydrogenase (SDH), Ca2+ handling, membrane potential (ΔÑ°m), and H2O2 production. ND decreased the latency for the first attack and increased the number of attacks by the resident mice against the intruder, mechanistically associated with an increase in glutamate levels and pGluN2BTyr1472 but not pGluN2ATyr1244, and GLT-1 downregulation. The abnormalities in mitochondrial Ca2+ influx, SDH, ΔÑ°m, and H2O2 implies in deficient energy support to the synaptic machinery. The ND/CEF group displayed a decreased aggressive behavior, normalization of glutamate and pGluN2BTyr1472levels, and mitochondrial function at synaptic terminals. In conclusion, the pharmacological modulation of GLT-1 highlights its relevance as an astrocytic target against highly impulsive and aggressive phenotypes.

Anabolic-androgen steroids effects on bioenergetics responsiveness of synaptic and extrasynaptic mitochondria.

We hypothesized that supraphysiological administration of the anabolic-androgenic steroids (AAS) like testosterone (TEST) and nandrolone decanoate (NAND) might differentially affect synaptic and extrasynaptic components of mitochondrial bioenergetics, thereby resulting in memory impairment. Oil (VEH), NAND or TEST (15 mg/Kg) were daily administered to male CF-1 albino mice for 19-days. We evaluated in the synaptosomes and extrasynaptic mitochondria, Ca2+ influx/efflux, membrane potential ΔÑ°m, oxidative respiratory states, dehydrogenases activity, H2O2 production, Tau phosphorylation, and spatial memory in the Morris water maze (MWM). In synaptosomes, both AAS increased Ca2+ influx and Na+ dependent efflux. In extrasynaptic mitochondria, NAND increased the Ca2+ influx. NAND prominently impaired ΔÑ°m formation and dissipation in synaptosomal and extrasynaptic mitochondria, while the effect of TEST was less pronounced. TEST increased the Reserve Respiratory Capacity in synaptosomes, and NAND decreased dehydrogenases activity in synaptic and extrasynaptic mitochondria. Also, NAND increased H2O2 production by synaptosomes and extrasynaptic mitochondria. NAND increased pTauSer396 in synaptosomes. Both AAS did not impair memory performance on MWM. We highlight that high doses of NAND cause neurotoxic effects to components of synaptic and extrasynaptic mitochondrial bioenergetics, like calcium influx, membrane potential and H2O2 production. TEST was less neurotoxic to synaptic and extrasynaptic mitochondrial bioenergetics responses.

Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration.

Traumatic brain injury (TBI) increases Ca2+ influx into neurons and desynchronizes mitochondrial function leading to energy depletion and apoptosis. This process may be influenced by brain testosterone (TS) levels, which are known to decrease after TBI. We hypothesized that a TS-based therapy could preserve mitochondrial neuroenergetics after TBI, thereby reducing neurodegeneration. C57BL/6J mice were submitted to sham treatment or severe parasagittal controlled cortical impact (CCI) and were subcutaneously injected with either vehicle (VEH-SHAM and VEH-CCI) or testosterone cypionate (15 mg/kg, TS-CCI) for 10 days. Cortical tissue homogenates ipsilateral to injury were used for neurochemical analysis. The VEH-CCI group displayed an increased Ca2+-induced mitochondrial swelling after the addition of metabolic substrates (pyruvate, malate, glutamate, succinate, and adenosine diphosphate [PMGSA]). The addition of Na+ stimulated mitochondrial Ca2+ extrusion through Na+/Ca2+/Li+ exchanger (NCLX) in VEH-SHAM and TS-CCI, but not in the VEH-CCI group. Reduction in Ca2+ efflux post-injury was associated with impaired mitochondrial membrane potential formation/dissipation, and decreased mitochondrial adenosine triphosphate (ATP)-synthase coupling efficiency. Corroborating evidence of mitochondrial uncoupling was observed with an increase in H2O2 production post-injury, but not in superoxide dismutase (SOD2) protein levels. TS administration significantly reduced these neuroenergetic alterations. At molecular level, TS prevented the increase in pTauSer396 and alpha-Spectrin fragmentation by the Ca2+dependent calpain-2 activation, and decreased both caspase-3 activation and Bax/BCL-2 ratio, which suggests a downregulation of mitochondrial apoptotic signals. Search Tool for the Retrieval of Interacting Genes/Proteins database provided two distinct gene/protein clusters, "upregulated and downregulated," interconnected through SOD2. Therefore, TS administration after a severe CCI improves the mitochondrial Ca2+extrusion through NCLX exchanger and ATP synthesis efficiency, ultimately downregulating the overexpression of molecular drivers of neurodegeneration.

Serum Biomarkers and Clinical Outcomes in Traumatic Spinal Cord Injury: Prospective Cohort Study.

BACKGROUND: A plethora of reactive cellular responses emerge immediately after a traumatic spinal cord injury (SCI) and may influence the patient's outcomes. We investigated whether serum concentrations of neuron-specific enolase, interleukin-6, glial-derived neurotrophic factor, and neurotrophic growth factor reflect the acute-phase responses to different etiologies of SCI and may serve as predictive biomarkers of neurologic and functional outcomes. METHODS: Fifty-two patients were admitted to the intensive care unit after SCI due to traffic accidents, falls, and firearm wounds and had blood samples collected within 48 hours and 7 days after SCI. Thirty-six healthy subjects with no history of SCI were included as controls. Neurologic and functional status was evaluated on the basis of American Spinal Injury Association and Functional Independence Measure scores over a period of 48 hours and 6 months after SCI. RESULTS: Serum NSE increased significantly 48 hours and 7 days after SCI compared with controls, while interleukin-6 increased only at 48 hours. In contrast, the neurotrophic growth factor level significantly decreased 48 hours and 7 days after SCI. Serum glial-derived neurotrophic factor level did not differ from control at any time point. Also, there was no significant difference in biomarker concentrations between the etiologies of SCI or the level of spinal injury. There were no correlations between biomarker levels at 48 hours with neurologic or functional outcomes 7 days and 6 months after SCI. CONCLUSIONS: Our results suggest expansive axonal damage coupled with an acute proinflammatory response after SCI. However, in our study biomarker concentration did not correlate with short- or long-term prognosis, such as survival rate or sensory and motor function.

Acylated Ghrelin and Circulatory Oxidative Stress Markers Responses to Acute Resistance and Aerobic Exercise in Postmenopausal Women.

BACKGROUND: Since exercise increases the production of reactive oxygen species in different tissues, the objective of this study is to evaluate, compare and correlate the acute effects of aerobic and resistance exercise in circulatory markers of oxidative stress and acylated ghrelin (AG) in postmenopausal women. METHODS: Ten postmenopausal women completed different protocols: a control session (CON), an aerobic exercise session (AERO); and a single-set (SSR) or 3-set (MSR) resistance exercise protocol. RESULTS: After exercise, both MSR (P = .06) and AERO (P = .02) sessions showed significant increased lipid peroxidation compared with baseline levels. CON and SSR sessions showed no differences after exercise. No differences were found between sessions at any time for total glutathione, glutathione dissulfide or AG concentrations. CONCLUSIONS: Exercise significantly increased lipid peroxidation compared with baseline values. As pro oxidant stimuli is necessary to promote chronic adaptations to the antioxidant defenses induced by exercise, our findings are important to consider when evaluating exercise programs prescription variables aiming quality of life in this population.

The effects of diet- and diet plus exercise-induced weight loss on basal metabolic rate and acylated ghrelin in grade 1 obese subjects.

BACKGROUND: Diet and exercise are often prescribed as primary intervention regarding obesity-related disorders. Additionally, recent studies have shown beneficial effects of weight loss through diet and exercise in ghrelin concentrations in obese subjects. The aim of this study was to evaluate the effects of a 5% weight loss on lipid profile, resting metabolic rate (RMR), and acylated ghrelin (AG) using two different methods of intervention (diet or diet plus exercise). MATERIALS AND METHODS: Eighteen subjects (twelve women and six men) aged 20-40 years with a body mass index of 30-34.9 kg/m(2) (grade 1 obesity) were randomized into two intervention groups: diet (n=9) or diet plus exercise (n=9). Both groups underwent treatment until 5% of the initial body weight was lost. At baseline and upon completion, RMR and AG were analyzed. RESULTS: Both groups showed a significant decrease in body fat percentage and fat mass. The diet-plus-exercise group showed a decrease in AG (pre: 54.4±25.3 pg/mL and post: 33.2±19.1 pg/mL) and an increase in RMR (pre: 1,363±379 kcal/day, post: 1,633±223 kcal/day). CONCLUSION: These data suggest that diet plus exercise induced weight loss and had beneficial effects on AG concentration and RMR, essential factors to ensure the benefits of a weight-loss program.