CDC in brief 2013

With the start of the 113th Congress, we\u2019d like to take an opportunity to (re)introduce the Centers for Disease Control and Prevention (CDC), and provide some helpful information about our agency and its work. This E-Brief contains links to useful information about CDC\u2019s science, budget, and presence on the ground. For quick access to additional information about CDC\u2019s work, please contact the CDC Washington Office at (202) 245-0600, and see below for information about how CDC Washington can help you.CS238048-6What CDC does -- Fast facts -- CDC on the ground -- How can CDC Washington help you?201

Effect of Rhodiola Rosea extracts on binge eating in female rats

Stress is a determinant of binge eating. Rhodiola rosea (ROR) extracts modulate stress responses. The present study evaluated the effect ofRORdry extract and its active principles in rats in which binge eating for highly palatable sweet food (HPF) was evoked by stress and repeated food restrictions. Female Sprague–Dawley rats were submitted to three 8-day cycles of food restriction/refeeding (4 d 66% of the usual chow intake, 4 d food ad libitum) and to acute stress on d25. Stress was induced by preventing access to HPF for 15 min, while rats were able to see and smell it. 4 groups of rats were used: NR+NS rats were normally fed and not stressed on the test day (d25); NR+ S rats were similarly fed but were stressed on d25; R +NS rats were exposed to 3 cycles of yo-yo dieting but not stressed; R + S rats were exposed to 3 cycles of yo-yo dieting and stressed on d25. ROR dry extract (containing 3% rosavin and 3.12% salidroside) or the purified principles were given by gavage 1 h before access to HPF. Food restrictions and stress induced binge eating in R + S rats, increasing HPF intake of about 50% in the first 15 min. 10 mg/kg of ROR extract significantly reduced and 20 mg/kg abolished the HPF binge in R + S rats, but did not modify HPF intake in NR+ NS, NR+ S or R +NS rats. Rosavin or salidroside, 600 or 636g/kg (i.e. the amounts in 20 mg/kg of extract) significantly reduced HPF intake in R + S rats; when given together they completely abolished the binge response. Thus, ROR extracts or its active principles, rosavin and salidroside, may be interesting agents for treatment of bingeing-related eating disorders

A preclinical model of binge eating elicited by yo-yo dieting and stressful exposure to highly palatable food

Preclinical models are needed to investigate the neurobiology and psychobiology of binge eating (BE) and to identify innovative pharmacotherapeutic strategies. BE episodes are characterized by uncontrollable, distressing eating of a large amount of highly palatable food (HPF). These episodes represent a central feature of bingeing-related eating disorders, such as binge eating disorder, bulimia nervosa, and binge/purge subtype anorexia nervosa. In line with the hypothesis that dieting and stress are key etiological determinants of BE the proposed model combines cycles of food restriction–refeeding and acute stress to evoke BE for sweet HPF. Four groups of female rats were employed: group 1 was normally fed and not stressed on the test day (25th); group 2 was fed normally but was exposed to an acute stress on day 25; group 3 was exposed to three cycles (4 days 66% of chow intake+4 days food ad libitum) of yo-yo dieting but not stressed; and group 4 was exposed to cyclic yo-yo dieting and then stressed. All groups were fed highly palatable food (HPF) for 2 h on days 5–6 and 13–14. Acute stress was elicited by exposing rats to HPF, but preventing them from access to it for 15 min, even though they were able to see it and to smell its odor. The combination of cyclic food restriction and stressful exposure to food markedly increased HPF intake. To test the predictive validity of this model, three drugs were evaluated: sibutramine, fluoxetine, and topiramate, chosen since clinical studies have reported that they may be effective in the treatment of bingeing-related eating disorders. Topiramate selectively inhibited compulsive HPF intake in rats submitted to caloric restriction and stress, thus, its effect was evident only in conditions in which binge-type eating occurred. Sibutramine and fluoxetine inhibited food intake in all conditions suggesting that their effect is a general effect on appetite and/or satiety and is not selective on the binge-type behavior. Midazolam was included to assess whether an anxiolytic benzodiazepine might reduce BE in response to a stressful procedure. Midazolam did not modify binge eating BE rats, but increased HPF intake in the other three groups of rats, as previously observed in animals and humans. Pharmacological results suggest that this model, in addition to face validity as an isomorphic model of human binge eating, is endowed with good predictive validity. Thus, the present model may be useful to evaluate new pharmacological strategies for the treatment of bingeing related eating disorders

Effect of the selective CRF-1 receptor antagonist R121919 in an animal model of binge eating

Episodes of binge eating (BE) in humans are characterized by compulsive, non-homeostatic consumption of an unusually large quantity of highly palatable food (HPF) in a short period of time. Considerable evidence suggests that BE may be caused by a unique interaction between dieting and stress. The present study evaluated the effect of the corticotrophin releasing factor 1 receptor (CRF-1R) antagonist R121919 in female rats, in which BE for HPF was evoked by stress and repeated food restrictions (Cifani et al. (2009) Psychopharmacology 204:113-25). The model employs female rats in relation to the higher prevalence of binge eating disorders in women than in men. Four groups of female Sprague-Dawley rats were used: NR+NS was normally fed and not stressed on the test day (d25); NR+S was fed as NR+NS and stressed on d25; R+NS was exposed to 3 cycles of yo-yo dieting (8-day cycles of food restriction/refeeding (4d 66% of the standard chow food intake, 4d food ad libitum) but not stressed; R+S was fed as R+NS and stressed on d25. All groups were fed HPF for 2 h on day 5-6 and 13-14. Stress was induced by preventing access to HPF for 15 min, while rats were able to see and smell it. After the stressful procedure the rats had free access to HPF and standard chow. R121919 was injected subcutaneously 1 h before access to HPF. BE was selectively observed in R+S, that showed a marked increase in HPF intake in comparison to NR+NS. Intake of standard chow pellets was not significantly modified. HPF intake in R+NS and NR+S was not significantly different from that of NR+NS. R121919 (10-20 mg/kg) significantly reduced HPF intake in R+S, but had no effect in the other 3 groups. After the stressful procedure, rats showed increased serum corticosterone (CORT) levels. To asses whether CORT is involved in the BE response, R+S and NR+NS were treated with metyrapone, a CORT synthesis inhibitor at the doses of 50 and 100 mg/kg. It failed to prevent BE. Lastly, CORT injection (2.5 and 10 mg/kg) did not induce BE in R+NS, in comparison to NR+NS. These findings suggest that CRF-1R mechanisms are involved in the BE response following stress and food restrictions; this effect is likely related to its extrahypothalamic functions rather than to its regulatory role in HPA axis activity