Steven J. Wickler

Thermogenic capacity and brown fat in rats exercise-trained by running

Brown adipose tissue, a major effector of nonshivering thermogenesis (NST) in mammals, is activated by the sympathetic neurotransmitter norepinephrine. Prolonged increases in norepinephrine levels, whether elicited by cold exposure or exogenous application of catecholamines, lead to increased NST and increased thermogenic capacity of brown fat. Exercise training is also accompanied by enhanced sympathetic activity. The possibility exists that this enhancement may alter brown fat function. The present study was designed to assess the effect of a running exercise regimen on whole animal NST and the in vivo response of brown fat. Rats were trained by running on a treadmill (an average of 17 m/min, 0 degrees incline, for 90 min/d) for a period of at least 6 weeks. Whole animal NST capacity was assessed by monitoring oxygen consumption in response to infusion of norepinephrine. As a measure of the contribution of brown fat to whole body NST, the mass and norepinephrine-stimulated blood flow (microsphere technique) to the tissue were measured. None of these variables differed between the exercised (n = 10) and sedentary (n = 10) groups. That is, there were no significant differences between the two groups with respect to resting oxygen consumption, norepinephrine-induced oxygen consumption, brown fat mass, and brown fat blood flow--whether expressed per gram of tissue or as total tissue blood flow (ie, tissue mass X blood flow per gram). Further study is needed to explain the differential responses of brown fat to the increased sympathetic activity occurring during exercise v that occurring during cold exposure.

Muscle function in hibernating hamsters: A natural analog to bed rest?

Abstract 1. 1. In Experiment I(fall/winter), hamsters exposed to cold and short photoperiod entered hibernation; hamsters exposed to cold and long photoperiod did not. 2. 2. Hibernators had reduced body masses, significantly atrophied skeletal muscles, but increased mass-specific maximum activities of citrate synthase (an indicator of aerobic capacity) and HOAD (an indicator of β-oxidation). 3. 3. In Experiment II (winter/spring), hamsters were similarly exposed to cold and either long or short photoperiods, but none hibernated. 4. 4. No differences occurred in skeletal muscle masses or enzymatic activities of these two nonhibernating groups in Experiment II. 5. 5. Thus, photoperiod per se does not appear to elicit the skeletal muscle changes seen in the hibernating hamsters; nor are these changes comparable to those seen during bed or limb immobilization.

Lipoprotein lipase activity and cellularity in brown and white adipose tissue in Zucker obese rats

The genetically obese adult Zucker rat (fafa) exhibits reduced thermogenesis when stimulated by physiological agents (cold, catecholamines). Recent evidence suggests that this thermogenic defect may be important in the manifestation of the animals obesity and that it reflects a reduced thermogenic contribution from brown adipose tissue, the major nonshivering thermogenic site in many mammals. The present study describes the effects of the obese genotype on brown (and white) adipocyte size, number, and lipid content and tissue lipoprotein lipase (LPL) activity. In the obese rats, brown fat depots were increased in mass. This increase could be accounted for by brown fat hypertrophy (due primarily to an increase in the amount of triglyceride present in each cell) rather than hyperplasia (there being no increase in the number of brown fat cells). In addition, unlike the situation in white fat, the brown fat from the obese rats did not exhibit higher LPL activity than did the brown fat from their lean littermates. This absence of an increased capacity for triglyceride uptake, coupled with the greater amount of triglyceride per brown adipocyte, is consistent with a reduction of triglyceride oxidation (and, thus, heat production) in the cells from the obese (v the lean) rats.

Nonshivering thermogenesis and brown fat in spontaneously hypertensive rats

Oxygen consumption was measured before and during infusion of the catecholamine isoproterenol in age-matched spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats. Mass-independent rates of oxygen consumption of anesthetized 7-week-old rats were similar in the WKY and SHR rats (11.08 +/- 0.74 and 11.33 +/- 0.82 ml O2 min-1 kg-.67, respectively). Catecholamine infusion elicited increased total oxygen consumption in both WKY and SHR animals (15.0 +/- 1.0 and 14.9 +/- 1.2 ml O2 min-1 kg-.67, respectively), and the magnitude of these increases did not significantly differ. To assess whether there were changes in the metabolic state of brown adipose tissue, the major site of catecholamine-induced thermogenesis in rats, enzymes whose activity is proportional to aerobic capacity were assayed in vitro. In both the interscapular and cervical brown fat depots, maximal citrate synthase and maximal HOAD (beta-hydroxyacyl-CoA dehydrogenase) activities were similar in SHR and WKY rats. There were also no significant differences in brown fat protein content, suggesting no differential growth of this tissue in the two rat strains. Our results indicate that the nonshivering thermogenic capacity of the hypertensive SHR rats does not differ from that of the normotensive WKY animals.

Diminished Respiratory Responses of Brown Adipocytes Isolated from BIO 14.6 Dystrophic Hamsters

Abstract Catecholamine-induced thermogenesis is significantly diminished in BIO 14.6 cardiomyopathy hamsters as demonstrated by a reduced increase in oxygen consumption of these hamsters in response to administered isoproterenol. This decreased responsiveness is accompanied by a reduction in the amount of brown adipose tissue, a major nonshivering thermogenic effector. The present study demonstrates that the metabolic responses of individual brown fat cells are also altered in the dystrophic hamster. That is, 1 μM norepinephrine, the physiological mediator of nonshivering thermogenesis, evoked rates of oxygen consumption that were significantly lower in brown adipocytes isolated from the BIO 14.6 hamsters than in those from normal controls. Additionally, the dystrophic adipocytes exhibited: decreased maximal activity (per cell as well as per milligram protein) of citrate synthase; decreased cell size; and decreased amounts of protein per cell. These data indicate that the nonshivering thermogenic capacity of the intact BIO 14.6 hamsters reflects altered characteristics of the individual brown adipocytes themselves, as well as decreased amounts of the tissue.