The conditions of some biochemical and functional systems of the rat organisms at daily intramuscular injections of obsidan (0.05 mg/100 g body weight) for one month were studied to evaluate the effect of obsidan on the adrenergic-dependent adaptive reactions. It was shown that the procedure of injections itself (the control group of animals receiving injections of sodium chloride isotonic solution) is stress leading to a decrease of beta-adrenergic-dependent reactions and an increase of alpha-adrenergic-dependent ones. The combination of this stress with the pharmacological effect of obsidan is characterized by a decrease of adrenaline release in blood, a reduction of manifestations of alpha-adrenergic reactions, a decline of lipid energy substrates consumption level.
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Nature
July 2023
Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada.
Caloric restriction that promotes weight loss is an effective strategy for treating non-alcoholic fatty liver disease and improving insulin sensitivity in people with type 2 diabetes. Despite its effectiveness, in most individuals, weight loss is usually not maintained partly due to physiological adaptations that suppress energy expenditure, a process known as adaptive thermogenesis, the mechanistic underpinnings of which are unclear. Treatment of rodents fed a high-fat diet with recombinant growth differentiating factor 15 (GDF15) reduces obesity and improves glycaemic control through glial-cell-derived neurotrophic factor family receptor α-like (GFRAL)-dependent suppression of food intake.
View Article and Find Full Text PDFCirc Cardiovasc Imaging
May 2019
Pulmonary and Critical Care Section, VA Loma Linda Healthcare System, Loma Linda, CA (J.D.A., C.G., P.S.).
Background: Left ventricular (LV) twist mechanics are augmented with both acute and chronic hypoxemia. Although the underlying mechanisms remain unknown, sympathetic activation and a direct effect of hypoxemia on the myocardium have been proposed, the latter of which may produce subendocardial dysfunction that is masked by larger subepicardial torque. This study therefore sought to (1) determine the individual and combined influences of β-AR (β-adrenergic receptor) stimulation and peripheral O saturation (Spo) on LV twist in acute and chronic hypoxia and (2) elucidate whether endocardial versus epicardial mechanics respond differently to hypoxia.
View Article and Find Full Text PDFNat Commun
April 2018
Division of Metabolic Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.
In acute cold stress in mammals, JMJD1A, a histone H3 lysine 9 (H3K9) demethylase, upregulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals have another mechanism to cope with long-term cold stress by inducing the browning of the subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic-dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A.
View Article and Find Full Text PDFCogn Neuropsychiatry
May 2006
Institute of Neurology, London, UK.
Introduction: To survive, an organism must remember occurrences of value in its environment. These include those that pose a threat to survival, novel or unexpected stimuli, or a general class of stimuli that represent punishment or reward. There is substantial evidence that memory for novel and emotionally salient events is enhanced relative to familiar or emotionally neutral events.
View Article and Find Full Text PDFPflugers Arch
March 2005
Department of Internal Medicine, State University of Campinas, Brazil.
During cold exposure, homeothermic animals mobilize glucose with higher efficiency than at thermoneutrality. An interaction between the insulin signal transduction machinery and high sympathetic tonus is thought to play an important role in this phenomenon. In the present study, rats were exposed to cold during 8 days and treated, or not, with a beta3-adrenergic agonist, BRL37344 sodium 4-2-2-(3-chlorophenyl)-2-hydroxyethyl amino propyl phenoxy-acetic acid sodium (BRL37344), or antagonist, SR59230A 3-(2-ethylphenoxy)-[(1S)-1,2,3,4-tetrahydronaphth-1-ylamino]-(2S)-2-propanol oxalate (SR59230A), to evaluate the cross-talk between insulin and beta3-adrenergic intracellular signaling in brown adipose tissue.
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