Intervention Strategies for Prevention of Comorbid Depression Among Individuals With Type 2 Diabetes: A Scoping Review

Background: Type 2 diabetes (T2D)-related depression has a significant impact on quality of life and leads to greater morbidity and mortality. Current educational and treatment programs for T2D rarely include a specific depression-prevention component, focusing largely on remediating depressive symptoms that have reached clinical levels.Objective: Given the vast field of research on the association between T2D and depression, and the unknown status of prevention efforts for the latter, the goal of this scoping review was to conduct a synopsis of intervention strategies specifically targeting the prevention of depression among adults with T2D.Eligibility Criteria: (1) participants aged 18 and over with T2D; (2) experimental and quasi-experimental designs (3) intervention strategies seeking to prevent the onset or worsening of (non-clinical) depressive symptoms; (4) a valid measure of depressive symptoms; (5) full-text articles available in English or French.Sources of Evidence: Databases including Medline, PubMed, and SCOPUS were searched between 2000 and 2018 resulting in 4,219 potential articles.Charting Methods: This review was conducted in-line with the current methodological framework for scoping reviews. Titles, abstract and full text articles were screened independently and in duplicate. A narrative analysis was conducted to synthesize study characteristics and the nature of intervention strategies and components.Results: Twelve studies were identified with the primary aim of preventing the incidence of depressive symptoms or improving non-clinical depression levels. Individual and group-based approaches included educational interventions incorporating diabetes self-management, problem-solving, and resilience-focused approaches, emotion-targeted techniques as well as alternative interventions. Self-monitoring, home practices, and motivational interviewing were common elements.Conclusions: This review lays the groundwork for future studies seeking to develop, validate, and improve prevention strategies targeting the diabetes-depression comorbidity. More studies over longer periods and with larger samples are needed to capture the effects of prevention efforts

Editorial: Rising stars in exercise physiology

[Extract] Physical exercise has been recognized as essential for human health and evolution for thousands of years, beginning with the ancient cultures. Hippocrates, Plato, Aristotle, and the Roman physician Galen were the earliest recorded and most well-known promoters of the beneficial effects of physical exercise. Since these times, several dedicated laboratories worldwide have been established, with many researchers conducting numerous investigations related to exercise physiology; nevertheless, a cornerstone of all laboratories is the development of new and novel researchers. These talented and emerging researchers have been necessary for our understanding of exercise physiology to have reached where we are today (and where we will be in the future). Given the evolution of exercise physiology, the field has incorporated a range of basic to applied scientific investigations and a range of end-users (e.g., researchers, athletes, coaches, physiologists, and clinical/public health professionals) who will benefit from these new advances in exercise physiology

Implication des lipides intramusculaires dans le développement de l'insulinorésistance chez des patients obèses et diabétiques de type 2

MONTPELLIER-BU Médecine UPM (341722108) / SudocMONTPELLIER-BU Médecine (341722104) / SudocSudocFranceF

Exercice physique et insulinorésistance : de la physiopathologie métabolique musculaire à l'intervention thérapeutique

L'insulinorésistance qui caractérise l'obésité et le diabète de type 2 est liée à des facteurs génétiques et environnementaux. La sédentarité joue un rôle déterminant dans le développement de l'insulinorésistance et le muscle des patients obèses ou diabétiques de type 2 présente de nombreuses anomalies qui portent sur le métabolisme des glucides et des lipides. La pratique régulière de l'exercice physique par ses effets bénéfiques sur le muscle et notamment sur la fonction mitochondriale constitue un bon moyen de prévention et une thérapeutique efficace dans l'obésité et le diabète de type 2

A role for maternally derived myokines to optimize placental function and fetal growth across gestation

Exercise during pregnancy is associated with improved health outcomes for both mother and baby, including a reduced risk of future obesity and susceptibility to chronic diseases. Overwhelming evidence demonstrates a protective effect of maternal exercise against fetal birth weight extremes, reducing the rates of both large- and small-for-gestational-age infants. It is speculated that this protective effect is mediated in part through exercise-induced regulation of maternal physiology and placental development/function. However, the specific mechanisms through which maternal exercise regulates these changes remain to be discovered. We hypothesize that myokines, a collection of peptides and cytokines secreted from contracting skeletal muscles during exercise, may be an important missing link in the story. Myokines are known to reduce inflammation, improve metabolism and enhance macronutrient transporter expression/activity in various tissues of non-pregnant individuals. Little research to date has focused on the specific roles of the myokine secretome in the context of pregnancy; however, it is likely that myokines secreted from exercising skeletal muscles may modulate the maternal milieu and directly impact the vital organ of pregnancy - the placenta. In the current review, data in strong support of this potential role of myokines will be presented, suggesting myokine secretion as a key mechanism through which maternal exercise optimizes fetal growth trajectories. It is clear that further research is warranted in this area, as knowledge of the biological roles of myokines in the context of pregnancy would better inform clinical recommendations for exercise during pregnancy and contribute to the development of important therapeutic interventions.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

The effects of bisphenol A and bisphenol S on adipokine expression and glucose metabolism in human adipose tissue

Purpose The environmental endocrine disruptors, bisphenol A (BPA) and bisphenol S (BPS) are associated with the development of type 2 diabetes. We aim to study the effects of BPA or BPS exposure on adipokine expression in human adipose tissue and on adipocyte glucose uptake. Methods Human subcutaneous adipose tissue was treated for 24 or 72 h with environmentally-relevant and supraphysiological concentrations of BPA or BPS (1–104 nM). Following exposure, gene expression of proinflammatory cytokines, adipokines, and estrogen receptors was measured in adipose tissue. Glucose uptake and the insulin signalling pathway were analyzed in isolated adipocytes following adipose tissue culture with BPA for 24 h. Results Adipose tissue treated with BPA for 24 h had reduced expression of the proinflammatory genes (IL6, IL1B, TNFA) and adipokines (ADIPOQ, FABP4). BPA and BPS had no effect on the expression of other proinflammatory genes (IL33), adipokines (LEP), or receptors (ESR1, ESR2) after 72-h exposure. Adipose tissue treated with environmentally-relevant concentrations of BPA for 24 h had reduced insulin-stimulated glucose uptake, without altered gene and protein levels of key insulin signalling pathway markers. Conclusions We found that human adipose tissue treated with environmentally-relevant concentrations of BPA for 24 h, but not BPS, reduced expression of proinflammatory genes and adipokines. Furthermore, BPA reduced glucose uptake in adipocytes independently of insulin signalling. Such mechanisms can contribute to the development of insulin resistance associated with BPA exposure

Exercise training reduces circulating cytokines in male patients with coronary artery disease and type 2 diabetes: A pilot study

Abstract Low‐grade inflammation is central to coronary artery disease (CAD) and type 2 diabetes (T2D) and is reduced by exercise training. The objective of this study was to compare the anti‐inflammatory potential of moderate‐to‐vigorous intensity continuous training (MICT) and high‐intensity interval training (HIIT) in patients with CAD with or without T2D. The design and setting of this study is based on a secondary analysis of registered randomized clinical trial NCT02765568. Male patients with CAD were randomly assigned to either MICT or HIIT, with subgroups divided according to T2D status (non‐T2D‐HIIT n = 14 and non‐T2D‐MICT n = 13; T2D‐HIIT n = 6 and T2D‐MICT n = 5). The intervention was a 12‐week cardiovascular rehabilitation program consisting of either MICT or HIIT (twice weekly sessions) and circulating cytokines measured pre‐ and post‐training as inflammatory markers. The co‐occurrence of CAD and T2D was associated with increased plasma IL‐8 (p = 0.0331). There was an interaction between T2D and the effect of the training interventions on plasma FGF21 (p = 0.0368) and IL‐6 (p = 0.0385), which were further reduced in the T2D groups. An interaction between T2D, training modalities, and the effect of time (p = 0.0415) was detected for SPARC, with HIIT increasing circulating concentrations in the control group, while lowering them in the T2D group, and the inverse occurring with MICT. The interventions also reduced plasma FGF21 (p = 0.0030), IL‐6 (p = 0.0101), IL‐8 (p = 0.0087), IL‐10 (p < 0.0001), and IL‐18 (p = 0.0009) irrespective of training modality or T2D status. HIIT and MICT resulted in similar reductions in circulating cytokines known to be increased in the context of low‐grade inflammation in CAD patients, an effect more pronounced in patients with T2D for FGF21 and IL‐6

Galactose enhances oxidative metabolism and reveals mitochondrial dysfunction in human primary muscle cells.

Human primary myotubes are highly glycolytic when cultured in high glucose medium rendering it difficult to study mitochondrial dysfunction. Galactose is known to enhance mitochondrial metabolism and could be an excellent model to study mitochondrial dysfunction in human primary myotubes. The aim of the present study was to 1) characterize the effect of differentiating healthy human myoblasts in galactose on oxidative metabolism and 2) determine whether galactose can pinpoint a mitochondrial malfunction in post-diabetic myotubes.Oxygen consumption rate (OCR), lactate levels, mitochondrial content, citrate synthase and cytochrome C oxidase activities, and AMPK phosphorylation were determined in healthy myotubes differentiated in different sources/concentrations of carbohydrates: 25 mM glucose (high glucose (HG)), 5 mM glucose (low glucose (LG)) or 10 mM galactose (GAL). Effect of carbohydrates on OCR was also determined in myotubes derived from post-diabetic patients and matched obese non-diabetic subjects. OCR was significantly increased whereas anaerobic glycolysis was significantly decreased in GAL myotubes compared to LG or HG myotubes. This increased OCR in GAL myotubes occurred in conjunction with increased cytochrome C oxidase activity and expression, as well as increased AMPK phosphorylation. OCR of post-diabetic myotubes was not different than that of obese non-diabetic myotubes when differentiated in LG or HG. However, whereas GAL increased OCR in obese non-diabetic myotubes, it did not affect OCR in post-diabetic myotubes, leading to a significant difference in OCR between groups. The lack of an increase in OCR in post-diabetic myotubes differentiated in GAL was in relation with unaltered cytochrome C oxidase activity levels or AMPK phosphorylation.Our results indicate that differentiating human primary myoblasts in GAL enhances aerobic metabolism. Because this cell culture model elicited an abnormal response in cells from post-diabetic patients, it may be useful in further studies of the molecular mechanisms of mitochondrial dysfunction