Certain hormonal changes after adrenaline injection in the obese

ABSTRACT

Obesity is the commonest metabolic abnormality in man. Several metabolic disturbances associated with obesity, have been reported. Although fasting plasma free fatty acids are higher in the obese compared to lean persons, injection of adrenalin evoked less fatty acid mobilizations in the obese than in the lean persons. The actual mechanisms underling this abnormality is certainly multifactorial, including several hormonal inter-relationships. The aim of this work is to compare the effect of adrenaline injection on the fasting serum concentration of T3, T4, TSH, cortisol and ACTH all intimately related to lipolysis between the obese and lean persons. Thirty-four obese persons, with an age range between 15-45 years, were compared to lean persons of almost the same age range. All subjects were carefully examined to ensure they are enjoying good health, and diabetes mellitus was excluded by a normal fasting and 2 h. postprandial blood sugar. Obesity was assessed using the body mass index and triceps skinfold thickness. Following a 12 hour [overnight] fast, serum levels of T3, T4, TSH, cortisol and ACTH were determined in all volunteers. Adrenaline [0.5 mg S.C.] was then injected in every participant and the postadrenaline serum level of the same hormones was determined. The haemodynamic responses to adrenaline were also measured in each participant in this experiment. The results demonstrated, that the fasting serum cortisol and ACTH were significantly higher in the obese as compared to lean persons. Both the lean and obese persons showed a significant haemodynamic response to S.C. adrenaline administration. Also, although the serum level of T3 and cortisol were significantly reduced in lean persons after S.C. adrenaline administration this failed to occur in the obese. These results clearly point to the multiple hormonal interrelationships and alterations in obesity, which probably underly many of the observed metabolic disturbances in obesity. Obesity has long been associated with insulin resistance. The mechanism although far from being estbalished, has been linked to a combined receptor and postreceptor defect. Recently, obese persons were also found to be resistant to the B. adrenergic mechanisms and hence the metabolic effects of catecholamines. Our results support the concept that hormonal alterations other than insulin are also involved in the obesity associated metabolic disturbances. The exact mechanisms are beyond the scope of this study