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1.
Levosulpiride for the treatment of diabetic macular oedema: a phase 2 randomized clinical trial.
Núñez-Amaro, CD, López, M, Adán-Castro, E, Robles-Osorio, ML, García-Franco, R, García-Roa, M, Villalpando-Gómez, Y, Ramírez-Neria, P, Pineiro, N, Rubio-Mijangos, JF, et al
Eye (London, England). 2024;(3):520-528
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Abstract
BACKGROUND/OBJECTIVE The prokinetic levosulpiride elevates vasoinhibin levels in the vitreous of patients with proliferative diabetic retinopathy (PDR) suggesting clinical benefits due to the anti-vasopermeability and anti-angiogenic properties of vasoinhibin. We investigated the biological activity of levosulpiride in centre-involving diabetic macular oedema (DME). PATIENTS/METHODS Prospective, randomized, double-blinded, dual-centre, phase 2 trial in patients with centre-involving DME orally treated with placebo (n = 17) or levosulpiride (n = 17) for 8 weeks or in patients with PDR undergoing elective pars plana vitrectomy and receiving placebo (n = 18) or levosulpiride (n = 18) orally for the 1 week before vitrectomy. RESULTS Levosulpiride improved changes from baseline in best-corrected visual acuity (p ≤ 0.037), central foveal thickness (CFT, p ≤ 0.013), and mean macular volume (MMV, p ≤ 0.002) at weeks 4, 6, and 8 compared to placebo. At 8 weeks, the proportion of eyes gaining ≥5 ETDRS letters at 4 m (41% vs. 28%), losing ≥21 μm in CFT (55% vs. 28%), and dropping ≥0.06 mm3 in MMV (65% vs. 29%) was higher after levosulpiride than placebo. The overall grading of visual and structural parameters improved with levosulpiride (p = 0.029). Levosulpiride reduced VEGF (p = 0.025) and PlGF (p = 0.008) levels in the vitreous of PDR patients. No significant adverse side-effects were detected. CONCLUSIONS Oral levosulpiride for 8 weeks improved visual and structural outcomes in patients with centre-involving DME by mechanisms that may include intraocular upregulation of vasoinhibin and downregulation of VEGF and PlGF. Larger clinical trials evaluating long-term efficacy and safety are warranted.
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Assessment of nurses' level of knowledge of the management of chronic wounds.
Fernández-Araque, A, Martinez-Delgado, M, Jiménez, JM, López, M, Castro, MJ, Gila, EC
Nurse education today. 2024;:106084
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Abstract
BACKGROUND Chronic wounds are a challenge and a major cause of morbidity. A wound is considered chronic if healing does not occur within the expected time frame depending on the etiology and location of the wound. OBJECTIVE To assess the level of knowledge about chronic wound management of postgraduate nurses in different areas of the health system and their previous satisfaction with the training received during their undergraduate studies. DESIGN Cross-sectional study of a health system of 95,000 inhabitants and 557 nursing professionals working in it. PARTICIPANTS Nurses working in the study health system and in areas with care for patients with chronic wounds in social, primary and hospital care. RESULTS Survey results described a low knowledge of chronic wound management in general. Data on knowledge according to area of work showed that nurses in primary care had the highest knowledge of wound etiology. Nurses working in health and social care were most knowledgeable in diagnostic knowledge. Hospital nurses showed the lowest knowledge overall. A relationship was observed when nurses had a master's degree followed by an expert with better knowledge in the test. In addition, nurses reported little training in chronic wounds during their university studies (69.73 %, n = 106). CONCLUSIONS Therefore, a review of this point should be considered to improve the management of chronic wounds and their correct approach among nursing students. A review of continuing and even specialised training needs in the clinical care setting should also be considered.
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Peripheral and central macrophages in obesity.
Mukherjee, S, Skrede, S, Haugstøyl, M, López, M, Fernø, J
Frontiers in endocrinology. 2023;:1232171
Abstract
Obesity is associated with chronic, low-grade inflammation. Excessive nutrient intake causes adipose tissue expansion, which may in turn cause cellular stress that triggers infiltration of pro-inflammatory immune cells from the circulation as well as activation of cells that are residing in the adipose tissue. In particular, the adipose tissue macrophages (ATMs) are important in the pathogenesis of obesity. A pro-inflammatory activation is also found in other organs which are important for energy metabolism, such as the liver, muscle and the pancreas, which may stimulate the development of obesity-related co-morbidities, including insulin resistance, type 2 diabetes (T2D), cardiovascular disease (CVD) and non-alcoholic fatty liver disease (NAFLD). Interestingly, it is now clear that obesity-induced pro-inflammatory signaling also occurs in the central nervous system (CNS), and that pro-inflammatory activation of immune cells in the brain may be involved in appetite dysregulation and metabolic disturbances in obesity. More recently, it has become evident that microglia, the resident macrophages of the CNS that drive neuroinflammation, may also be activated in obesity and can be relevant for regulation of hypothalamic feeding circuits. In this review, we focus on the action of peripheral and central macrophages and their potential roles in metabolic disease, and how macrophages interact with other immune cells to promote inflammation during obesity.
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Obesity wars: may the smell be with you.
López, M, Fernández-Real, JM, Tomarev, SI
American journal of physiology. Endocrinology and metabolism. 2023;(6):E569-E576
Abstract
Classically, the regulation of energy balance has been based on central and peripheral mechanisms sensing energy, nutrients, metabolites, and hormonal cues. Several cellular mechanisms at central level, such as hypothalamic AMP-activated protein kinase (AMPK), integrate this information to elicit counterregulatory responses that control feeding, energy expenditure, and glucose homeostasis, among other processes. Recent data have added more complexity to the homeostatic regulation of metabolism by introducing, for example, the key role of "traditional" senses and sensorial information in this complicated network. In this regard, current evidence is showing that olfaction plays a key and bidirectional role in energy homeostasis. Although nutritional status dynamically and profoundly impacts olfactory sensitivity, the sense of smell is involved in food appreciation and selection, as well as in brown adipose tissue (BAT) thermogenesis and substrate utilization, with some newly described actors, such as olfactomedin 2 (OLFM2), likely playing a major role. Thus, olfactory inputs are contributing to the regulation of both sides of the energy balance equation, namely, feeding and energy expenditure (EE), as well as whole body metabolism. Here, we will review the current knowledge and advances about the role of olfaction in the regulation of energy homeostasis.
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The combined effect of front-of-package labels and influencer recommendations on food choice decisions.
Sicilia, M, López, M, Palazón, M
Appetite. 2023;:107074
Abstract
Many governments have adopted front-of-pack nutrition labels (FOP labels) that give advice about how healthy a product is. An increasing number of digital food influencers are also informing consumers about the nutritional quality of products and promoting healthy consumption. In this context, the current study analyzes how both sources of information come together to affect purchase intention. Drawing on congruence theory, we propose that the influencer's recommendation reinforces the effect of the FOP label when there is congruence between the two; however, consumers clearly prefer to follow the recommendation of the influencer over the FOP label when the information sources are non-congruent. We develop a between-subjects experimental design in which the level of congruence between the two information sources is manipulated. The effect of the influencer on purchase intention is mediated by the credibility of the FOP label. A second study confirms the superiority of the influencer effect observed in the first study.
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Obesity wars: hypothalamic sEVs a new hope.
Mukherjee, S, Diéguez, C, Fernø, J, López, M
Trends in molecular medicine. 2023;(8):622-634
Abstract
There are currently several pharmacological therapies available for the treatment of obesity, targeting both the central nervous system (CNS) and peripheral tissues. In recent years, small extracellular vesicles (sEVs) have been shown to be involved in many pathophysiological conditions. Because of their special nanosized structure and contents, sEVs can activate receptors and trigger intracellular pathways in recipient cells. Notably, in addition to transferring molecules between cells, sEVs can also alter their phenotypic characteristics. The purpose of this review is to discuss how sEVs can be used as a CNS-targeted strategy for treating obesity. Furthermore, we will evaluate current findings, such as the sEV-mediated targeting of hypothalamic AMP-activated protein kinase (AMPK), and discuss how they can be translated into clinical application.
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Hypothalamic AMPK as a possible target for energy balance-related diseases.
López, M
Trends in pharmacological sciences. 2022;(7):546-556
Abstract
Hypothalamic AMP-activated protein kinase (AMPK) is a canonical regulator of energy balance and metabolism at the whole-body level. This makes this enzyme an attractive target for treating energy balance-related diseases. However, targeting AMPK within the hypothalamus presents a challenge related to the specific cellular biodistribution of the enzyme and the need to use clinically safe methods of administration. Current evidence has shown that targeting based on small extracellular vesicles (sEVs) might offer a realistic approach for regulating hypothalamic AMPK. This would allow modulation of both sides of the energy-balance equation, namely food intake and energy expenditure, and therefore of overall metabolism. Moreover, this strategy could provide treatment options not only for obesity but also for catabolic/wasting diseases such as hyperthyroidism, rheumatoid arthritis, and even cancer cachexia.
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Nicotine' actions on energy balance: Friend or foe?
Seoane-Collazo, P, Diéguez, C, Nogueiras, R, Rahmouni, K, Fernández-Real, JM, López, M
Pharmacology & therapeutics. 2021;:107693
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Abstract
Obesity has reached pandemic proportions and is associated with severe comorbidities, such as type 2 diabetes mellitus, hepatic and cardiovascular diseases, and certain cancer types. However, the therapeutic options to treat obesity are limited. Extensive epidemiological studies have shown a strong relationship between smoking and body weight, with non-smokers weighing more than smokers at any age. Increased body weight after smoking cessation is a major factor that interferes with their attempts to quit smoking. Numerous controlled studies in both humans and rodents have reported that nicotine, the main bioactive component of tobacco, exerts a marked anorectic action. Furthermore, nicotine is also known to modulate energy expenditure, by regulating the thermogenic activity of brown adipose tissue (BAT) and the browning of white adipose tissue (WAT), as well as glucose homeostasis. Many of these actions occur at central level, by controlling the activity of hypothalamic neuropeptide systems such as proopiomelanocortin (POMC), or energy sensors such as AMP-activated protein kinase (AMPK). However, direct impact of nicotine on metabolic tissues, such as BAT, WAT, liver and pancreas has also been described. Here, we review the actions of nicotine on energy balance. The relevance of this interaction is interesting, because considering the restricted efficiency of obesity treatments, a possible complementary approach may focus on compounds with known pharmacokinetic profile and pharmacological actions, such as nicotine or nicotinic acetylcholine receptors signaling.
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Impact of Preoperative Total Proteins and Glycated Hemoglobin on Recurrences after Early Colorectal Cancer.
Castro, MJ, Jiménez, JM, López, M, Cao, MJ, Santos-Torres, J, López, A, Moreno, A, Ruiz-Tovar, J
Nutrients. 2021;(2)
Abstract
BACKGROUND The outcome of colorectal cancer is mostly based on TNM classification. There are several factors determining that patients with the same tumoral stage present different outcomes. The nutritional status has been related to the immunological response and may affect the oncologic results. The purpose of this study was to determine if preoperative nutritional parameters may predict the oncologic outcome in patients with early colorectal cancer. METHODS A prospective observational study of patients undergoing elective surgery for colorectal cancer was performed with stage I. Preoperative nutritional assessment included glycemic and lipid profiles, total proteins, and albumin levels. These parameters were correlated with tumoral recurrence during a follow-up of at least 24 months. RESULTS During the period of study, 744 patients were operated on and 228 (30.6%) followed the inclusion criteria for this study. Recurrence rate was 5.7% (13 patients). Patients with hypoproteinemia showed a 7.8-fold greater risk of recurrence during the first 24 months after surgery [OR 7.8 (CI95% 1.3-48), p = 0.012]. Patients with glycated hemoglobin levels (HbA1c) > 6.2% showed a 2.3 increased risk of recurrence [OR 2.3 (CI95% 1.1-4.7; p = 0.01]. CONCLUSIONS Preoperative values of total proteins and HbA1c correlate with the recurrence rate in early colorectal cancer.
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Understanding the Effects of Antipsychotics on Appetite Control.
Mukherjee, S, Skrede, S, Milbank, E, Andriantsitohaina, R, López, M, Fernø, J
Frontiers in nutrition. 2021;:815456
Abstract
Antipsychotic drugs (APDs) represent a cornerstone in the treatment of schizophrenia and other psychoses. The effectiveness of the first generation (typical) APDs are hampered by so-called extrapyramidal side effects, and they have gradually been replaced by second (atypical) and third-generation APDs, with less extrapyramidal side effects and, in some cases, improved efficacy. However, the use of many of the current APDs has been limited due to their propensity to stimulate appetite, weight gain, and increased risk for developing type 2 diabetes and cardiovascular disease in this patient group. The mechanisms behind the appetite-stimulating effects of the various APDs are not fully elucidated, partly because their diverse receptor binding profiles may affect different downstream pathways. It is critical to identify the molecular mechanisms underlying drug-induced hyperphagia, both because this may lead to the development of new APDs, with lower appetite-stimulating effects but also because such insight may provide new knowledge about appetite regulation in general. Hence, in this review, we discuss the receptor binding profile of various APDs in relation to the potential mechanisms by which they affect appetite.