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[en] Highlights: • Seven weeks of Compound D159687 (D159687) induces weight loss in aged mice. • D159687 causes a selective loss of fat mass while preserving lean mass. • The weight loss in D159687 treated mice occurred despite increased food intake. Therapies that recapitulate the health benefits of caloric restriction in older adults are needed. Phosphodiesterase 4 inhibitors demonstrate such promise. We examined their effects on body weight and composition, physical and cognitive function in aged mice using Compound D159687 (D159687).
[en] Currently, a lot of space and time is devoted to the therapy of oncologic diseases itself. To reach the good therapy results, complex care of the oncologic patient is needed. Management of complications linked with the disease itself and management of complications emerged after administration of chemotherapy, radiotherapy or targeted therapy, plays a significant role. In addition to infectious, hematological, neurological, cardiac or other complications, metabolic complications are relatively extensive and serious. One of the most frequent metabolic complications in oncology is tumor lysis syndrome, hyperuricemia, hypercalcaemia and syndrome of inappropriate secretion of antidiuretic hormone. (author)
[en] Cognitive impairment is a brain dysfunction characterized by neuropsychological deficits in attention, working memory, and executive function. Maternal obesity and consumption of a high-fat diet (HFD) in the offspring has been suggested to have detrimental consequences for offspring cognitive function through its effect on the hippocampus and prefrontal cortex. Therefore, our study aimed to investigate the effects of maternal obesity and offspring HFD exposure on the brain metabolome of the offspring.
[en] Tyrosine phosphorylation of GPRC5B and phosphorylation-dependent recruitment of Fyn through the SH2 domain have been implicated in NF-κB activation and obesity-linked adipose inflammation. GPRC5B tightly associates with caveolin-1 (Cav1); however, the role of this interaction remains elusive. Here, we report that Cav1 reduces GPRC5B-mediated NF-κB signaling by blocking GPRC5B-phosphorylation. We demonstrate highly abundant tyrosine phosphorylation of GPRC5B is observed in Neuro2a cells lacking endogenous Cav1 expression. Reversely, exogenous expression of Cav1 in these cells inhibits GPRC5B-phosphorylation. Although GPRC5B lacks conventional caveolin-binding motif, cytoplasmic tail of GPRC5B directly interacts with the C-terminal domain of Cav1. The vacant scaffolding domain of Cav1 in the protein complex suggests a potential mechanism for blocking GPRC5B-phosphorylation by Cav1, because Fyn loses the activity by binding with Cav1-scaffolding domain. Enhanced GPRC5B-mediated NF-κB signaling in Cav1-deficient cells were observed under palmitate-induced metabolic stress. These results support Cav1 functions as a negative modulator for GPRC5B action.
[en] The aim of this study was to compare the variations in the concentrations of tocopherols and retinol in obese adults in the postprandial state after the intake of a Mediterranean or Western-style breakfast. The study was designed as a randomized, controlled intervention trial in the postprandial state, for which 24 male adults (12 obese and 12 of normalweight) were recruited. After a fat challenge, blood samples were collected at different times postprandially and α-tocopherol, γ-tocopherol and retinol concentrations were determined in serum by HPLC. The Mediterranean-style meal produced a greater increase in serum α-tocopherol levels in both obese and normal-weight subjects, compared to the Western-style meal, indicating that the composition of the food affects the concentration of tocopherols in the postprandial state. However, the serum concentrations of γ-tocopherol and retinol remained unmodified. In conclusion, the presence of α-tocopherol in the meal could contribute to the protection of the Mediterranean-style meal against atherosclerosis in the postprandial state.
[es]El objetivo de este estudio fue comparar las variaciones en la concentración de tocoferoles y retinol en adultos obesos en el estado postprandial tras la ingesta de un desayuno mediterráneo u occidental. Consiste en un ensayo de intervención aleatorio y controlado, en el que participaron 24 adultos varones (12 obesos y 12 normopeso). Tras la ingesta de dichas comidas, se determinaron las concentraciones de α-tocoferol, γ-tocoferol y retinol en el suero de las muestras sanguíneas mediante HPLC. La comida de estilo mediterráneo aumentó los niveles séricos de α-tocoferol en sujetos obesos y de peso normal, en comparación con una comida de estilo occidental, lo que indica que la composición del alimento afecta a su concentración sérica. Sin embargo, referente al γ-tocoferol y retinol, permanecieron sin modificaciones. En conclusión, la presencia de α-tocoferol en una comida de estilo mediterráneo podría contribuir a la protección contra la aterosclerosis en el estado postprandial
[en] Highlights: • Atf3 knockout mice increases body weight and impaired glucose tolerance in high fat diet fed mice. • Atf3 knockout mice increases body weight in chow diet fed aged mice. • Sulfuretin, a phytochemical Atf3 iducer, requires Atf3 expression to prevent obesity. Activating transcription factor 3 (Atf3) has been previously demonstrated to impact obesity and metabolism. However, a metabolic role of Atf3 in mice remains debatable. We investigated the role of Atf3 in mice and further investigated Atf3 expression as a therapeutic target for obesity and metabolic diseases. Atf3 knockout (KO) mice fed with a high fat diet (HFD) aggravated weight gain and impaired glucose metabolism compared to littermate control wild type (WT) mice. Atf3 KO aged mice fed with a chow diet (CD) for longer than 10 months also displayed increased body weight and fat mass compared to WT aged mice. We also assessed requirements of Atf3 in a phytochemical mediated anti-obese effect. Effect of sulfuretin, a previously known phytochemical Atf3 inducer, in counteracting weight gain and improving glucose tolerance was almost completely abolished in the absence of Atf3, indicating that Atf3 induction can be a molecular target for preventing obesity and metabolic diseases. We further identified other Atf3 small molecule inducers that exhibit inhibitory effects on lipid accumulation in adipocytes. These data highlight the role of Atf3 in obesity and further suggest the use of chemical Atf3 inducers for prevention of obesity and metabolic diseases.
[en] Obesity has become a global problem due to its sharply increased prevalence and associated complications. Orexin and opioid signaling can regulate feeding behavior and represent potential therapeutic targets for obesity. In the present experiment, we sought to ascertain the effects of orexin-A and μ-opioid signaling regulation in the basomedial amygdala (BMA) on feeding and investigate the physiology of gastric distension (GD)-responsive neurons in a diet-induced obesity (DIO) and diet-induced obesity resistance (DR) rat model. Intra-BMA infusions of orexin-A increased the firing of BMA GD neurons and increased food intake, and that these effects could be abolished by pretreatment with the orexin-1 receptor (OX-1R) antagonist SB334867, these effects could also be somewhat attenuated by co-administration of naloxone. In the DIO and DR rats, mRNA expression of OX-1R and μ-opioid receptors were increased in the BMA. Our results strongly suggest that orexin-A and opioid signaling in the BMA play a major role in regulating GD neuronal excitability and feeding behavior in obesity.