1,720,994 research outputs found
Front-of-pack (FOP) labelling systems, nutrition education, and obesity prevention: nutri-score and nutrinform battery need more research
No full textEvidence for the existence of two distinct dopamine D-2 receptors in presynaptic nerve terminals from rat corpus striatum
No full text1 Radioactive rubidium (86Rb+) efflux was used to measure potassium (K+) permeability in a study designed to assess both the presence and the sensitivity to ions and drugs of the K+ channels in the presynaptic nerve terminals of rat striatum. This method allowed differential measurement of the activity of two distinct components of 86Rb+ efflux, component V (sensitive to voltage and Ca2+-independent) and component C (Ca2+-activated). 2 A series of dopamine D-2 receptor agonists, including quinpirole, bromocriptine and Ru 24213, appeared to affect both components of 86Rb+ efflux. The EC50 values of quinpirole, bromocriptine and Ru 24213 for activating component V of 86Rb+ efflux were 5 pM, 15 pM and 40 pM, respectively. These drugs also stimulated component C of 86Rb+ efflux in the same order, but with lower, potency. 3 The dopaminergic D-2 agonist BHT 920 discriminated between the two components being active on component V (EC50 = 200 pM) and inactive on component C (up to 1 - μM). 4 Activation of voltage-sensitive 86Rb+ efflux by various dopamine D-2 receptor agonists, including BHT 920, were antagonized by 0.1 μM (-)-sulpiride but not by 0.1 μM yohimbine. 5 Lesioning of the nigro-striatal pathway by injection of 6-hydroxydopamine in the substantia nigra caused a reduction of about 60% of the BHT 920-stimulated, voltage-sensitive, Ca2+ independent 86Rb+ efflux (component V). 6 These data indicate that striatal presynaptic nerve terminals contain two distinct dopamine D-2 receptors which can be differentiated both functionally and pharmacologically
Role of sympathetic activity in controlling the expression of vascular endothelial growth factor in brown fat cells of lean and genetically obese rats
No full textStriatal adenylate cyclase-inhbiting dopamine D2 receptors are not affected by the aging process
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Amino acids contribute to adaptive thermogenesis. New insights into the mechanisms of action of recent drugs for metabolic disorders are emerging
Full text linkAdaptive thermogenesis is the heat production by muscle contractions (shivering thermogenesis) or brown adipose tissue (BAT) and beige fat (non-shivering thermogenesis) in response to external stimuli, including cold exposure. BAT and beige fat communicate with peripheral organs and the brain through a variegate secretory and absorption processes − controlling adipokines, microRNAs, extracellular vesicles, and metabolites − and have received much attention as potential therapeutic targets for managing obesity-related disorders. The sympathetic nervous system and norepinephrine-releasing adipose tissue macrophages (ATM) activate uncoupling protein 1 (UCP1), expressed explicitly in brown and beige adipocytes, dissolving the electrochemical gradient and uncoupling tricarboxylic acid cycle and the electron transport chain from ATP production. Mounting evidence has attracted attention to the multiple effects of dietary and endogenously synthesised amino acids in BAT thermogenesis and metabolic phenotype in animals and humans. However, the mechanisms implicated in these processes have yet to be conclusively characterized. In the present review article, we aim to define the principal investigation areas in this context, including intestinal microbiota constitution, adipose autophagy modulation, and secretome and metabolic fluxes control, which lead to increased brown/beige thermogenesis. Finally, also based on our recent epicardial adipose tissue results, we summarise the evidence supporting the notion that the new dual and triple agonists of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon (GCG) receptor − with never before seen weight loss and insulin-sensitizing efficacy − promote thermogenic-like amino acid profiles in BAT with robust heat production and likely trigger sympathetic activation and adaptive thermogenesis by controlling amino acid metabolism and ATM expansion in BAT and beige fat
Childhood obesity, overweight and underweight: a study in primary schools in Milan.
No full textThe study aims to assess the prevalence of obesity, overweight and underweight in children enrolled in government primary schools (6-11 years of age) in the city of Milan, Italy.One hundred and nine schools were randomly selected for the study. A cross-sectional study was conducted between March and June 2008. A survey was conducted using 16,588 questionnaires completed by parents. Anthropometric data (reported) of both parents and children and information on levels of physical activity and time children spent watching television (TV) were obtained.In the total sample, parents are predominantly (75.0 \%) of normal weight (M: 55.2 \%; F: 79.1 \%), 16.8 \% are overweight (M: 36.9 \%; F: 12.6 \%), 4.0 \% are obese (M: 6.6 \%; F: 3.5 \%) and 4.2 \% are underweight (M: 1.3 \%; F: 4.8 \%). Among children, 68.7 \% are of normal weight (M: 68.2 \%; F: 69.2 \%), 14.7 \% are overweight (M: 15.3 \%; F: 14.2 \%), 4 \% are obese (M: 4.5 \%; F: 3.4 \%), 11.8 \% are underweight (M: 11.2 \%; F: 12.5 \%) and 0.8 \% are severely thin (M: 0.9 \%; F: 0.7 \%). Children practice physical activity once or twice/week (48.3 \%), three to four times/week (38.9 \%) or five to seven times/week (8.9 \%), while 3.9 \% of children do not do any exercise. Most children (85.3 \%) watch TV from 30 min to 2 h/day.Contrary to the reported national average, the study shows the presence of only moderate levels of above-average weight and obesity among children. However, it remains important to monitor this phenomenon to raise awareness and to design programs of prevention throughout the country
Multiple symmetric lipomatosis may be the consequence of defective noradrenergic modulation of proliferation and differentiation of brown fat cells.
No full textMultiple symmetric lipomatosis (MSL) is an inherited disorder in which enlarging and unencapsulated lipomas symmetrically develop in the subcutaneous tissue of the neck, shoulders, mammary, and truncal regions. In some cases, it is associated with mitochondrial DNA abnormalities. The pathogenesis of MSL is completely unknown, although the fat deposits may be due to a neoplastic-like proliferation of functionally defective brown adipocytes. It has recently been demonstrated that the beta(3)-adrenergic receptor is the functionally relevant adrenergic receptor subtype in brown adipocytes and that its stimulation by noradrenaline (NA) modulates the expression of genes, such as uncoupling protein (UCP)-1 and inducible nitric oxide synthase (iNOS), involved in fat cell proliferation and differentiation. Furthermore, Trp64Arg mutation of the beta(3)-adrenoceptor has been implicated in lower NA activity in adipose tissues. The aim of this study was to investigate the molecular and functional characteristics of MSL adipocytes and to analyse the effects of nitric oxide (NO) on the proliferation/differentiation of MSL adipocytes in culture, and the relevance of putative noradrenergic deficit in the development of lipomas in MSL patients. Cultured MSL adipocytes were able to synthesize UCP-1 (the selective marker of brown adipocytes), but unlike that of normally functioning brown fat cells, the expression of the UCP-1 gene was not significantly induced by NA. NA is also defective in inducing iNOS gene expression, thus leading to reduced NO production and a consequent reduction in the anti-proliferative, adipogenic (mitochondrial biogenesis) effects of NA on MSL cells. Furthermore, the transcriptional peroxisome proliferator-activated receptor gamma co-activator-1 (PGC-1), which plays a key role in the sympathetic-stimulated mitochondrial biogenesis of brown adipocytes, is expressed but not induced by NA in MSL cells, as it is in brown adipocytes. The study did not find any association between beta(3)-adrenoceptor gene polymorphism and noradrenergic signalling defects in MSL subjects with or without mitochondrial DNA mutations
Dopamine inhibition of neurotensin-induced increase in Ca2+ influx into rat pituitary cells.
No full textIn this paper, we report that the intracellular mechanism by which neurotensin stimulates prolactin release involves an increase in Ca2+ uptake by pituitary cells rather than an effect on adenylate cyclase system. In addition, dopamine can prevent neurotensin-induced calcium influx by interacting with dopamine D2-receptors which appear to be completely independent of the adenylate cyclase moiety but are coupled to calcium channels
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