759 research outputs found
Removal of a large fragment of rhodopsin without changes in its spectral properties, by proteolysis of retinal rod outer segments
Localisation of the major site of light stimulated phosphorylation in a region of rhodopsin distinct from the chromophore binding site
Oxygen in metabolic dysfunction and its therapeutic relevance
Significance: In recent years, a number of studies have shown altered oxygen partial pressure at a tissue level in metabolic disorders, and some researchers have considered oxygen to be a (macro) nutrient. Oxygen availability may be compromised in obesity and several other metabolism-related pathological conditions, including sleep apnea-hypopnea syndrome, the metabolic syndrome (which is a set of conditions), type 2 diabetes, cardiovascular disease, and cancer. Recent Advances: Strategies designed to reduce adiposity and its accompanying disorders have been mainly centered on nutritional interventions and physical activity programs. However, novel therapies are needed since these approaches have not been sufficient to counteract the worldwide increasing rates of metabolic disorders. In this regard, intermittent hypoxia training and hyperoxia could be potential treatments through oxygen-related adaptations. Moreover, living at a high altitude may have a protective effect against the development of abnormal metabolic conditions. In addition, oxygen delivery systems may be of therapeutic value for supplying the tissue-specific oxygen requirements. Critical Issues: Precise in vivo methods to measure oxygenation are vital to disentangle some of the controversies related to this research area. Further, it is evident that there is a growing need for novel in vitro models to study the potential pathways involved in metabolic dysfunction to find appropriate therapeutic targets. Future Directions: Based on the existing evidence, it is suggested that oxygen availability has a key role in obesity and its related comorbidities. Oxygen should be considered in relation to potential therapeutic strategies in the treatment and prevention of metabolic disorders
The influence of GDP on Ca2+ uptake by mitochondria of brown adipose tissue from lean and genetically obese (ob/ob) mice
Hypoxia and adipose tissue function and dysfunction in obesity
The rise in the incidence of obesity has led to a major interest in the biology of white adipose tissue. The tissue is a major endocrine and signalling organ, with adipocytes, the characteristic cell type, secreting a multiplicity of protein factors â the adipokines. Increases in the secretion of a number of adipokines occurs in obesity, underpinning inflammation in white adipose tissue and the development of obesity-associated diseases. There is substantial evidence, particularly from animal studies, that hypoxia develops in adipose tissue as the tissue mass expands, and the reduction in pO2 is considered to underlie the inflammatory response. Exposure of white adipocytes to hypoxic conditions in culture induces changes in the expression of >1,000 genes. The secretion of inflammation-related adipokines is up-regulated by hypoxia, and there is a switch from oxidative metabolism to anaerobic glycolysis. Glucose utilisation is increased in hypoxic adipocytes with corresponding increases in lactate production. Importantly, hypoxia induces insulin resistance in fat cells and leads to the development of adipose tissue fibrosis. Many of the responses of adipocytes to hypoxia are initiated at pO2 levels above the normal physiological range for adipose tissue. The other cell types within the tissue also respond to hypoxia, with the differentiation of preadipocytes to adipocytes being inhibited and preadipocytes being transformed into leptin-secreting cells. Overall, hypoxia has pervasive effects on the function of adipocytes and appears to be a key factor in adipose tissue dysfunction in obesity
Upregulation of the expression of inflammatory and angiogenic markers in human adipocytes by a synthetic cannabinoid, JTE-907
Inflammation in adipose tissue is a characteristic
of obesity and the metabolic syndrome. It is
suggested that the endocannabinoid system is
involved in the regulation of infl ammatory and
angiogenic processes within the tissue. Human
subcutaneous preadipocytes (Zen Bio) were
used as the source of human preadipocytes or
adipocytes. Gene expression was examined
by RT-PCR and real-time PCR. The secretion of
infl ammation-related proteins was determined
by an ELISA array. In experiments on adipocytes
treated at day 14 post-diff erentiation, JTE-907, a
synthetic cannabinoid, upregulated the expression
of key infl ammatory markers â IL-6, MCP-1
and IL-1 β â and angiogenic factors â VEGF and
ANGPTL4 â at 10 Îź M after 20 h of treatment,
having also increased the expression of TRPV1
at 10 Îź M. JTE-907 showed no eff ect after 4 h.
The ELISA array showed a 2.6-fold increase in
IL-6 protein release. The eff ect of JTE-907 was
inhibited by AM251 (CB 1 antagonist), and partially
by arachidonyl serotonin (TRPV1 and FAAH
antagonist). The CB 2 antagonist, AM630, partially
upregulated the eff ect of JTE-907. Preadipocytes
fed 14 days after 100 % confl uence exhibited
downregulation of CB 1 , MCP-1, and IL-1 β , 20 h
after having been exposed to JTE-907. CB 1 and
TRPV1 receptors participate in the regulation
of several infl ammatory and angiogenic factors
in human adipocytes, indicating their potential
value as targets for the treatment of disorders
related to obesity
The influence of physical exercise on the generation of TGF-β1, PDGF-AA, and VEGF-A in adipose tissue
Adipose tissue is an important organ that produces and secretes hormones and cytokines, including TGF-β1, PDGF-AA, and VEGF-A. The goal of the present study was to investigate the influence of a single session of acute exercise, as well as the prolonged endurance training on the production of TGF-β1, PDGF-AA, and VEGF-A in the subcutaneous white adipose tissue in rats. Rats were randomly divided into two groups: untrained (UT, n = 30) and trained rats (T, subjected to 6-week endurance training with increasing load, n = 29). Both groups were subjected to an acute exercise session with the same work load. The rats were killed before (UTpre, Tpre), immediately after (UT0h, T0h), or 3 h (UT3h, T3h) after exercise and adipose tissue samples collected. Growth factor mRNA was evaluated using RT-PCR; the protein levels were measured before and after training (UTpre and Tpre) using the immunoenzymatic method. TGF-β1 and PDGF-AA mRNA levels were decreased in the UT3h rats compared to the UTpre rats (P = 0.0001 and P = 0.03, respectively), but the VEGF-A mRNA level remained unchanged in the UT0h and UT3h rats compared to UTpre rats. TGF-β1, PDGF-AA and VEGF-A mRNA levels were decreased in the T3h rats compared to Tpre (P = 0.0002, P = 0.02, and P = 0.03, respectively). TGF-β1, PDGF-AA and VEGF-A mRNA levels significantly increased in the Tpre rats compared to UTpre (all P = 0.0002). However, the protein levels remained constant. In conclusion, prolonged physical exercise increases growth factor mRNA in adipose tissue but not protein levels
GDP binding to brown-adipose-tissue mitochondria of mice treated chronically with corticosterone
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