We have previously shown that 6 weeks of intermittent high-fat diet (Int-HFD) pre-exposure significantly reduced alcohol drinking in rats, providing preliminary evidence of the effectiveness of a dietary intervention in reducing alcohol intake. However, the functional framework and underlying neurobiological mechanisms of such dietary intervention are unknown. Here, we examined the impact of Int-HFD pre-exposure duration on alcohol drinking, plasma feeding peptides, and central neurotransmitter receptors gene expression. Male Long Evans rats (n = 6–7/group) received no pre-exposure, 1 or 2 weeks pre-exposure to Int-HFD and alcohol drinking (two-bottle choice) was evaluated. We observed HFD pre-exposure-dependent decrease in alcohol drinking, with a significant decrease observed following 2 weeks of Int-HFD pre-exposure. No significant between-group differences in plasma feeding peptides (i.e., ghrelin, leptin, insulin) were detected. A PCR array revealed that the expression of several neurotransmitter receptors was significantly (p < 0.05 and ≥2-fold) altered in the striatum and ventral tegmental area compared to controls. These data suggest that pre-exposure to a palatable diet is critical to reduce alcohol drinking in rats, possibly through genetic alterations in the brain reward circuitry. Importantly, the present study is a step forward in identifying the critical framework needed to evaluate the therapeutic potential of nutritional contingency in the management of alcoholism.

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Appearance of secondary sexual development before the age of 9 in a male child and before the age of 7 in a female child is called precocious puberty. When the cause of precocious puberty is premature activation of the hypothalamic-pituitary axis, it is called central or complete precocious puberty, if ectopic gonadotrophin secretion occurs in boys or autonomous sex steroid secretion occurs in either sex it is called incomplete precocious puberty. |Here we are reporting a 5 year old girl with central precocious puberty.

Binge eating disorder (BED), the most common eating disorder in the US, has a lifetime prevalence of 2.8% and has been associated with many other psychological and metabolic disorders. Several preclinical models developed to study binge‐eating disorder and related pathologies use stress, food restriction, or limited access conditions to induce binge‐like intake. Using limited access model, Corwin and colleague, demonstrated that limited‐short (2 hr Mon, Wed and Fri) access to vegetable shortening induced a binge‐compensate feeding pattern which was not present in limited‐regular (2 hr every day) access conditions. Similar findings were reported when a nutritionally complete high‐fat diet was utilized either every day (HFD‐ED) or every‐third day (HFD‐3D). Using this model, we have recently shown that both HFD‐ED and HFD‐3D groups of rats undergo similar binge‐compensate eating patterns and display compulsive feeding/risk‐taking behavior, suggesting the frequency instead of presence/absence of binge‐like feeding episodes as a major difference between HFD‐3D and HFD‐ED. It was also unclear if the intermittent availability or the HFD itself triggered compulsive feeding. Therefore, in the present study, we evaluated the impact of ad libitum chow and western diet (WD; rich in both sugar and fat) consumed in a binge manner in relation to the same diet consumed in a non‐binge manner. Male Long Evans rats received chronic (every day) or intermittent (Mon, Wed, and Fri) 24 hr access to Western Diet for six weeks. The control group received normal rodents chow. All the animals had ad libitum access to chow and water throughout the experiment. We observed that intermittent access‐group significantly overconsumed on WD‐access days and under‐consumed on chow‐access days as compared to both chow controls and chronic access group. Chronic access group, on the other hand, significantly overconsumed every day as compared to chow controls but not in a binge/compensate manner. Only intermittent access‐group showed elevated food intake than their baseline during the first two hours of WD‐access days. Finally, only the intermittent access‐group showed risk‐taking behavior when tested in the light/dark box. These data demonstrate selective induction of risk‐taking behavior following binge‐like eating but not when the same diet was consumed in a non‐binge manner. Support or Funding Information Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number TL4GM118968 and RL5GM118966. This publication was also made possible by funding, in part, by NIMHD‐RCMI # G12MD007595‐10, NIGMS‐BUILD # UL1GM118967 and NIGMS‐SCORE # 1SC3GM127173‐01A1 to SS. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.