The sympathetic nervous system has been implicated in the regulation of glucose-induced thermogenesis in man. The present study was undertaken to examine the influence of a pharmacological beta blockade on the thermogenic response after ingestion of a mixed meal. Ten healthy male volunteers were examined on two occasions, once during intravenous administration of beta-blocking agent (Series 1) and once without (Series 2). Five subjects received propranolol and the other five atenolol. Two subjects were also studied on a third occasion after 1 week of other propranolol medication (Series 3). Continuous respiratory gas exchange measurements were carried out for 1 h in the basal state and then for 3 h postprandially. The subjects ingested a standardized test meal in liquid form. After the meal oxygen uptake and energy expenditure both rose markedly during the first hour and then reached a relatively stable plateau. The average increase in oxygen uptake above basal during the whole study period was 27.0 +/- 1.4 vs. 26.7 +/- 1.4% (NS) in Series 1 and 2, respectively. The corresponding values for energy expenditure were 28.6 +/- 1.4 vs. 28.6 +/- 1.6%. Also in absolute terms, the increments above basal did not differ between the two series. Moreover, the basal measurements and the response to the meal were no different in the subjects in Series 1 receiving the selective beta-1 antagonist and the non-selective blocker, respectively. In conclusion, the present findings indicate that in healthy man, beta-adrenergically mediated sympathetic nervous system activity does not significantly influence the magnitude of the thermogenic response to a mixed meal.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/j.1475-097x.1989.tb00986.x | DOI Listing |
Biochem Pharmacol
January 2025
Institute of Medical Research at the San Carlos Clinic Hospital (IdISSC), Madrid, Spain; Department of Cell Biology, Faculty of Medicine, Complutense University of Madrid, Spain.
PAS domain-containing serine/threonine-protein kinase (PASK) is a nutrient and energy sensor regulated by fasting/refeeding conditions in hypothalamic areas involved in controlling energy balance. In this sense, PASK plays a role in coordinating the activation/inactivation of AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) in response to fasting. PASK deficiency protects against the development of diet-induced obesity.
View Article and Find Full Text PDFNat Commun
January 2025
Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Obesity poses a global health challenge, demanding a deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role of the mitochondrial protein Methylation-controlled J protein (MCJ/DnaJC15) in orchestrating brown adipose tissue (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident in human and mouse adipose tissue samples.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
World-Class Scientific Center "Center for Personalized Medicine", Almazov National Medical Research Centre, 197341 St. Petersburg, Russia.
The failure of the fight against obesity makes us turn to new goals in its treatment. Now, brown adipose tissue has attracted attention as a promising target for the treatment of obesity and associated metabolic disorders such as insulin resistance, dyslipidemia, and glucose tolerance disorders. Meanwhile, the expansion of our knowledge has led to awareness about two rather different subtypes: classic brown and beige (inducible brown) adipose tissue.
View Article and Find Full Text PDFPLoS One
December 2024
Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Maidashi, Higashi-ku, Fukuoka, Japan.
Sci Signal
December 2024
Division of Gastroenterology and Hepatology, Joan & Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, NY 10065, USA.
Activation of thermogenic brown adipose tissue (BAT) and inducible beige adipose tissue (BeAT) is triggered by environmental or metabolic stimuli, including cold ambient temperatures and nutrient stress. Thioesterase superfamily member 1 (Them1), a long-chain fatty acyl-CoA thioesterase that is enriched in BAT, suppresses acute cold-induced thermogenesis. Here, we demonstrate that expression was induced in BAT and BeAT by the carbohydrate response element binding protein (ChREBP) in response to chronic cold exposure or to the activation of the integrated stress response (ISR) by nutrient excess.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!