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Introduction: Resistance training has been associated with improved insulin sensitivity in individuals with type 2 diabetes, but its role in non-diabetic overweight individuals remains unclear. This study aimed to evaluate whether progressive resistance training reduces insulin resistance in overweight men at high risk of developing type 2 diabetes. We hypothesized that such training would significantly improve insulin sensitivity markers. Methods: Thirteen overweight male individuals (aged 30-50 years, BMI > 25 kg/m2, HOMA-IR > 1.9 mg/kg and HbA1c < 5.8%) participated in an 8-week supervised resistance training program ( 3 sessions/week). Strength was measured using no more than one repetition of each exercise. Pre- and post-training assessments included Bioelectrical impedance analysis, fasting blood insulin (FBI), fasting blood glucose (FBG), total cholesterol, HbA1c and HOMA-IR. Results: A significant gain in muscle mass (pre: 35.21 ± 3.18 kg vs. post: 36.12 ± 2.91 kg, p< 0.001) and a decrease in fat mass (pre: 30.93 ± 1.88 kg vs. post: 30.17 ± 1.82 kg, p<0.001) were observed. Rates of insulin resistance decreased significantly as insulin sensitivity improved with decreased FBI (pre: 12.16 ± 1.88 vs. post: 11.64 ± 1.52 μUI/mL, p< 0.05), while FBG remained unchanged. HbA1c levels dropped from 5.37 ± 0.31% to 5.10 ± 0.34% (p < 0.001). HOMA-IR scores improved significantly (pre: 2.77 ± 0.50 vs. post: 2.57 ± 0.42, p < 0.001). Conclusion: In overweight Jordanian men at risk of developing type 2 diabetes, a resistance exercise program administered 3 times per week for 8 weeks can significantly improve insulin resistance. Introducción: El entrenamiento de resistencia se ha asociado con una mejor sensibilidad a la insulina en personas con diabetes tipo 2, pero su papel en personas con sobrepeso no diabéticas sigue siendo incierto. El objetivo de este estudio era evaluar si el entrenamiento de resistencia progresivo reduce la resistencia a la insulina en hombres con sobrepeso y alto riesgo de desarrollar diabetes tipo 2. Planteamos la hipótesis de que dicho entrenamiento mejoraría significativamente los marcadores de sensibilidad a la insulina. Métodos: trece hombres con sobrepeso (de 30 a 50 años, IMC > 25 kg/m², HOMA-IR > 1,9 mg/kg y HbA1c < 5,8 %) participaron en un programa de entrenamiento de resistencia supervisado de 8 semanas (3 sesiones por semana). La fuerza se midió utilizando el máximo de una repetición de cada ejercicio. Las evaluaciones previas y posteriores al entrenamiento incluyeron análisis de impedancia bioeléctrica, niveles de insulina en ayunas (FBI), glucemia en ayunas (FBG), colesterol total, HbA1c y HOMA-IR. Resultados: se observó un aumento significativo de la masa muscular (pre: 35,21 ± 3,18 kg vs. post: 36,12 ± 2,91 kg, p < 0,001) y una disminución de la masa grasa (pre: 30,93 ± 1,88 kg vs. post: 30,17 ± 1,82 kg, p < 0,001). Las tasas de resistencia a la insulina disminuyeron significativamente a medida que mejoraba la sensibilidad a la insulina, con una disminución de la FBI (pre: 12,16 ± 1,88 μIU/mL vs. post: 11,64 ± 1,52 μIU/mL, p < 0,05), mientras que la glucosa en ayunas (GA) no se alteró. Los niveles de HbA1c disminuyeron del 5,37 ± 0,31 % al 5,10 ± 0,34 % (p < 0,001). Las puntuaciones HOMA-IR mejoraron significativamente (2,77 ± 0,50 frente a 2,57 ± 0,42, p < 0,001). Conclusión: en hombres jordanos con sobrepeso y riesgo de desarrollar diabetes tipo 2, un programa de ejercicios de resistencia administrado tres veces por semana durante ocho semanas puede mejorar significativamente la resistencia a la insulina. Introdução: O treino de resistência tem sido associado à melhoria da sensibilidade à insulina em pessoas com diabetes tipo 2, mas o seu papel em indivíduos não diabéticos com excesso de peso permanece incerto.O objetivo deste estudo foi avaliar se o treino de resistência progressivo reduz a resistência à insulina em homens com excesso de peso e com alto risco de desenvolver diabetes tipo 2. A nossa hipótese é que tal treino melhoraria significativamente os marcadores de sensibilidade à insulina.Métodos: Treze homens com excesso de peso (com idades compreendidas entre os 30 e os 50 anos, IMC > 25 kg/m², HOMA-IR > 1,9 mg/kg e HbA1c < 5,8%) participaram num programa de treino de resistência supervisionado de 8 semanas (3 sessões por semana). A força foi medida através da repetição máxima de cada exercício. As avaliações pré e pós-formação incluíram a análise da impedância bioelétrica (BIA), insulina em jejum (FIG), glicemia em jejum (GJ), colesterol total, HbA1c e níveis de HOMA-IR.Resultados: Observou-se um aumento significativo da massa muscular (pré: 35,21 ± 3,18 kg vs. pós: 36,12 ± 2,91 kg, p < 0,001) e uma diminuição da massa gorda (pré: 30,93 ± 1,88 kg vs. pós: 30,17 ± 1,82 kg, p < 0,001). As taxas de resistência à insulina diminuíram significativamente à medida que a sensibilidade à insulina melhorou, com uma diminuição da FBI (pré: 12,16 ± 1,88 μIU/mL vs. pós: 11,64 ± 1,52 μIU/mL, p < 0,05), enquanto a glicemia em jejum (GJ) permaneceu inalterada. Os níveis de HbA1c diminuíram de 5,37 ± 0,31% para 5,10 ± 0,34% (p < 0,001). Os escores HOMA-IR melhoraram significativamente (2,77 ± 0,50 vs. 2,57 ± 0,42, p < 0,001). Conclusão: Em homens jordanos com excesso de peso e com risco de desenvolver diabetes tipo 2, um programa de exercício de resistência administrado três vezes por semana durante oito semanas pode melhorar significativamente a resistência à insulina.

Lipodystrophy (lipohypertrophy, lipoatrophy) is one of the most common complications of subcutaneous insulin injections. This paper presents the case of a 46-year-old patient with uncontrolled type 2 diabetes mellitus, treated with insulin glargine 45UI/day, no glycemic control and multiple adjustments and hospitalizations. On admission, self-monitoring showed off-target basal and postprandial values, baseline glucose of 299 mg/dL and HbA1c of 11%. Medical history revealed flaws in the technique used for insulin administration, particularly, lack of application site rotation. Physical examination allowed to observe lipohypertrophy caused by excess bilateral infraumbilical adipose panniculus and induration of the subcutaneous cellular tissue. Ultrasound exposed fat infiltration in anterior recti. The patient was instructed on the correct technique for applying insulin with daily rotation of the application site, and allowing the areas affected by lipohypertrophy to rest. A self-monitoring guide was also provided. Self-monitoring within the first 10 days showed improvement in baseline glucose levels up to 116 mg/dL and borderline value of 75 mg/dL, compared to the previous baseline blood glucose level of 242 mg/dL with the same type of insulin and dose. Close follow-up was done to define the required insulin dose and to monitor possible hypoglycemia, obtaining an improvement in HbA1c of 9.2% and 8.8% at 4 and 11 months, respectively.

This study aimed to demonstrate the long-term effects of high-intensity interval training (HIIT) on reducing blood glucose levels in patients with type 2 diabetes mellitus. The research employs a preexperimental design with a one-group pretest‒posttest design. A total of 20 patients with type 2 diabetes mellitus, aged 40–60 years, participated in the study and received the HIIT intervention three times per week for eight weeks. Data collection involved measuring fasting blood glucose levels before and after the HIIT intervention via the ONE TOUCH™ BASIC™ Plus Meter. Data analysis was conducted via paired sample t tests with a significance level of 5%, and the effect size was evaluated via Cohen's d. Paired sample t test analysis between pre-HIIT and post-HIIT blood glucose levels (181.50±17.85 mg/dL to 99.50±8.26 mg/dL, p ≤ 0.001) revealed a significant reduction, with a large effect size (Cohen's d = 5.896). This study confirms that long-term high-intensity interval training is effective in lowering fasting blood glucose levels to normal ranges in patients with type 2 diabetes mellitus. Keywords: Blood glucose, HIIT, insulin sensitivity, insulin resistance, type 2 diabetes patients

The relationship between metabolic health and breast cancer emerges as an expanding area of research in comparative oncology, particularly highlighted in studies conducted among humans and canines. This review explores how dietary habits, obesity, and metabolic syndromes influence the risk, progression, and response to breast cancer treatments. To this end, the impact of obesity, diet, and lifestyle on carcinogenesis mechanisms and prognosis in human and canine patients affected by mammary tumors is examined. By examining comparative studies addressing the relationship between metabolic health and breast cancer in women and canines, common molecular and biochemical pathways in both species are identified. This approach provides a broader understanding of oncological diseases and their development, suggesting potential strategies for the prevention, diagnosis, and treatment of breast cancer from a metabolic perspective. However, as this area of research is still developing, it is necessary to explore new research lines to fully understand the complex relationship between metabolic health and cancer across different species from biochemical, molecular, genetic, and epigenetic perspectives, with the goal of gaining valuable knowledge that contributes to the development of new diagnostic, prognostic, and therapeutic tools.

La hipertrigliceridemia es una de las causas de pancreatitis aguda, generalmente con un riesgo mayor cuando su valor supera los 1.000 mg/dl. Se han descrito diferentes alternativas terapéuticas para el tratamiento de pacientes con pancreatitis por hipertrigliceridemia, entre ellas la infusión de insulina. Se reporta el caso de un paciente con hipertrigliceridemia muy severa que presentó pancreatitis aguda y su evolución fue favorable con la terapia con insulina.

Human studies support the relationship between high intake of fructose-sweetened beverages and type 2 diabetes, but there is a debate on whether this effect is fructose-specific or it is merely associated to an excessive caloric intake. Here we investigate the effects of 2 months’ supplementation to female rats of equicaloric 10% w/v fructose or glucose solutions on insulin sensitivity in target tissues. Fructose supplementation caused hepatic deposition of triglycerides and changed the fatty acid profile of this fraction, with an increase in monounsaturated and a decrease in polyunsaturated species, but did not cause inflammation and oxidative stress. Fructose but not glucose-supplemented rats displayed an abnormal glucose tolerance test and did not show increased phosphorylation of V-akt murine thymoma viral oncogene homolog-2 (Akt) in white adipose tissue and liver after insulin administration. In skeletal muscle, phosphorylation of Akt and of Akt substrate of 160 kDA (AS160) was not impaired but the expression of the glucose transporter type 4 (GLUT4) in the plasma membrane was reduced only in fructose-fed rats. In conclusion, fructose but not glucose supplementation causes fatty liver without inflammation and oxidative stress and impairs insulin signaling in the three major insulin-responsive tissues independently from the increase in energy intake.

Until recently mental diseases were treated as a whole, without any differentiation. Recent researchs have highlighted the differences between some of them, so consequently there are specific treatments for these pathologies today. The main objective of this work is to show two different diseases which in many cases are confused: depression and schizophrenia. These pathologies can have as triggers situations very diverse and that require different treatment. For the analysis, we are going to use two films: Prozac Nation (2001) by Erik Skjoldbjaerg and A beautiful mind (2001) by Ron Howard, which reflect the real experiences of two characters; the society in which they live and the environment around them, but especially focusing in the pharmacotherapy area, medications used, its correct use, the adverse effects and so on; in order to be able to decide if the vision presented by films has a formative character in these diseases.

The purpose of this study is to highlight the impact of exercise on increasing GLUT4 translocation in cell membranes. This study searches many journal databases, including Embase, Pubmed, Web of Science, and Scopus, as part of a systematic review methodology. Publications released during the last five years and publications mentioning were the inclusion criteria for this study physical exercise, GLUT4 and glucose uptake. The study's exclusion criteria were publications that were published in not reputable journals. 508 papers in all were found using the databases Scopus, Web of Science Pubmed, and Embase. For this systematic review, a total of 10 papers that satisfied the inclusion criteria were chosen and examined. This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) evaluation guidelines for standard operations. The outcome of this comprehensive analysis study report that there is an increase and acceleration of GLUT4 translocation during physical exercise. This has the effect of increasing glucose uptake in the blood so that there is an increase in the need for glucose in the blood. We recommend that physical exercise be a preventive measure for each individual in terms of increasing blood glucose uptake which is useful for maintaining balanced glucose levels in the blood and maintain general body health. Keywords: Physical training; GLUT4; Glucose; Insulin

The development of new therapies to induce self-tolerance has been an important medical health challenge in type 1 diabetes. An ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side effects and allow β-cell regeneration. Based on the immunomodulatory effects of apoptosis, we hypothesized that apoptotic mimicry can help to restore tolerance lost in autoimmune diabetes. To generate a synthetic antigen-specific immunotherapy based on apoptosis features to specifically reestablish tolerance to β-cells in type 1 diabetes. A central event on the surface of apoptotic cells is the exposure of phosphatidylserine, which provides the main signal for efferocytosis. Therefore, phosphatidylserine-liposomes loaded with insulin peptides were generated to simulate apoptotic cells recognition by antigen presenting cells. The effect of antigen-specific phosphatidylserine-liposomes in the reestablishment of peripheral tolerance was assessed in NOD mice, the spontaneous model of autoimmune diabetes. MHC class II-peptide tetramers were used to analyze the T cell specific response after treatment with phosphatidylserine-liposomes loaded with peptides. We have shown that phosphatidylserine-liposomes loaded with insulin peptides induce tolerogenic dendritic cells and impair autoreactive T cell proliferation. When administered to NOD mice, liposome signal was detected in the pancreas and draining lymph nodes. This immunotherapy arrests the autoimmune aggression, reduces the severity of insulitis and prevents type 1 diabetes by apoptotic mimicry. MHC class II tetramer analysis showed that peptide-loaded phosphatidylserine-liposomes expand antigen-specific CD4+ T cells in vivo. The administration of phosphatidylserine-free liposomes emphasizes the importance of phosphatidylserine in the modulation of antigen-specific CD4+ T cell expansion. We conclude that this innovative immunotherapy based on the use of liposomes constitutes a promising strategy for autoimmune diseases.

Reprogramming acinar cells into insulin producing cells using adenoviral (Ad)-mediated delivery of Pdx1, Ngn3 and MafA (PNM) is an innovative approach for the treatment of diabetes. Here, we aimed to investigate the molecular mechanisms involved in this process and in particular, the role of microRNAs. To this end, we performed a comparative study of acinar-to-β cell reprogramming efficiency in the rat acinar cell line AR42J and its subclone B13 after transduction with Ad-PNM. B13 cells were more efficiently reprogrammed than AR42J cells, which was demonstrated by a strong activation of β cell markers (Ins1, Ins2, IAPP, NeuroD1 and Pax4). miRNome panels were used to analyze differentially expressed miRNAs in acinar cells under four experimental conditions (i) non-transduced AR42J cells, (ii) non-transduced B13 cells, (iii) B13 cells transduced with Ad-GFP vectors and (iv) B13 cells transduced with Ad-PNM vectors. A total of 59 miRNAs were found to be differentially expressed between non-transduced AR42J and B13 cells. Specifically, the miR-200 family was completely repressed in B13 cells, suggesting that these cells exist in a less differentiated state than AR42J cells and as a consequence they present a greater plasticity. Adenoviral transduction per se induced dedifferentiation of acinar cells and 11 miRNAs were putatively involved in this process, whereas 8 miRNAs were found to be associated with PNM expression. Of note, Ad-PNM reprogrammed B13 cells presented the same levels of miR-137-3p, miR-135a-5p, miR-204-5p and miR-210-3p of those detected in islets, highlighting their role in the process. In conclusion, this study led to the identification of miRNAs that might be of compelling importance to improve acinar-to-β cell conversion for the future treatment of diabetes.