Activity-based anorexia is characterized by suppressed food intake and excessive physical activity. These behaviors are typical of persons with anorexia nervosa. Activity of the hypothalamic-pituitary-adrenal axis is known to be elevated in anorexia nervosa. We investigated the status of this axis in activity-based anorexia. Meal fed-control (MFC) and meal fed-wheel running (MFWR) rats were given access to food for 90 min daily; MFWR animals were allowed access to an activity wheel the remainder of the day. The experiment terminated when MFWR animals reached 75% of preexperimental body weight (males 3.9 +/- 0.3 d; females 4.2 +/- 0.2 d). Male and female MFWR rats consumed less food than MFC animals, while maintaining a high level of wheel running. Corticosterone concentrations were significantly elevated in MFWR animals. Corticotropin-releasing hormone mRNA concentrations in the paraventricular nucleus were not different. Relative adrenal gland weights were greater and thymus gland weights were lower in MFWR animals. Changes in food intake could not be explained by differences in insulin, glucose, beta-hydroxybutyrate or norepinephrine concentrations. Our results suggest increased activity of the hypothalamic-pituitary-adrenal axis in activity-based anorexia.

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Thirty-five years ago, Lois and Theodore Zucker reported the discovery of a genetic mutation in the rat that resulted in juvenile-onset obesity, increased food intake, decreased energy expenditure, and insulin resistance. The mutation was called fatty (fa). The fatty gene is passed on to successive generations by an autosomal recessive mode of inheritance. In the intervening years, much work has been done to characterize the many abnormalities of this animal model of obesity. Nearly 10 years ago, we reviewed the evidence for a central nervous system mechanism in the etiology of obesity in the fatty Zucker rat. Since that time, the discovery of novel peptides and genes has revolutionized the study of the etiology of genetically linked obesities. In this review, we update the evidence for a central nervous system mechanism of obesity in Zucker rats by focusing on the possible role of neuropeptide Y (NPY) and leptin in the etiology of obesity. We also discuss the role of glucocorticoids and insulin in the regulation of NPY.

Abstract.A crossover from a non-Fermi liquid to a Fermi liquid phase in Yb 2 Ni 12 P 7 is observed by analyzing electrical resistivity ρ(T ), magnetic susceptibility χ(T ), specific heat C(T ), and thermoelectric power S(T ) measurements. The electronic contribution to specific heat, C e (T ), behaves as C e (T )/T ∼ − ln(T ) for 5 K < T < 15 K, which is consistent with non-Fermi liquid behavior. Below T ∼ 4 K, the upturn in C e (T )/T begins to saturate, suggesting that the system crosses over into a Fermi-liquid ground state. This is consistent with robust ρ(T )−ρ 0 = AT 2 behavior below T ∼ 4 K, with the power-law exponent becoming sub-quadratic for T > 4 K. A crossover between Fermiliquid and non-Fermi liquid behavior suggests that Yb 2 Ni 12 P 7 is in close proximity to a quantum critical point, in agreement with results from recent measurements of this compound under applied pressure.

5-Thioglucose (5-TG) has been shown to increase food intake after acute administration. To determine the longer-term effects of 5-TG on feeding and body composition, thirty-four female Sprague-Dawley rats were cannulated into the fourth ventricle and infused with artificial CSF and either 0.01 M 5-TG or 0.1 M 5-TG using osmotic pumps. Food intake and body weight were monitored daily. Rats were killed after 14 days of infusion. Carcass and fatpad weights were measured, and body compositions were determined. Food intake was not different during the first week of infusion; however, cumulative food intake was decreased in the 0.1 M 5-TG group during the second week as compared to the CSF control group. Body weight and carcass weight of this group also decreased as compared to the control. The group receiving the higher dose of 5-TG (0.1 M) had increased fatpad weights in all three depots examined (inguinal, retroperitoneal, and perimetrial depot); the group with lower dose of 5-TG infusion (0.01 M) increased the fatpad weights in the retroperitoneal and perimetrial depot, as compared to the CSF group. Data from the body composition analysis were consistent with the results of the fatpad weights. In conclusion, the present study demonstrated that chronic fourth ventricular 5-TG infusion increased body fat without increasing food intake, suggesting that energy expenditure is decreased under this condition. The results of this study indicate that glucose metabolism in the hindbrain is important in the control of energy expenditure, body fat deposition, and thus energy balance regulation.