Project description:To investigate the effects of DHA (omega-3) treatment on affecting brain dysfunction and metabolic disorders by profiling the transcripome in the hypothalamus of male Bgn_KO mice (with and without DHA) at 13 weeks old.
Project description:Gene Expressoin Profile in the Hypothalamus and Liver of Male Bgn_KO, FMOD_KO and WT Mice at 13 Weeks Old, With and Without DHA (omega-3) Treatment
Project description:To investigate the effects of gene Fmod on affecting brain dysfunction and metabolic disorders by profiling the transcripome in the hypothalamus and liver of male Fmod_KO mice at 13 weeks old.
Project description:To investigate the effects of gene Bgn on affecting brain dysfunction and metabolic disorders by profiling the transcripome in the hypothalamus of male Bgn_KO and wild-type (WT, litter mate) mice at 13 weeks old.
Project description:C57BL/6J male mice (11 weeks old) were randomly divided into two groups fed either the control (Con) diet (LabDiet 5010) or fiber deficiency (FD) diet for 15 weeks.
Project description:A control group of male C57BL/6J mice were fed a 60% fat diet (Research Diets D12492i) for 8 weeks, resulting in “ad libitum obesity” (ALO). Leptin receptor-deficient B6.BKS(D)-Leprdb/J (“db/db”) male mice were fed a low-fat chow diet (PicoLab Rodent Diet 20; Purina Mills Inc). Once the average body weights of the two groups were equivalent, all mice were fasted for 24 hours, after which they were sacrificed and perigonadal adipose tissue (PGAT) was dissected out. PGAT was cultured ex vivo for 6 hours, after which conditioned media was collected and submitted for proteomic profiling. At the time of sacrifice, ALO mice were 17 weeks old and db/db mice were 10 weeks old. “HFD” is also used to refer to the ALO condition while “DB” is used to refer to the “db/db” condition.
Project description:Systemic acute inflammatory signals can cause profound anorexia by disrupting the physiological appetite regulation in the hypothalamic milieu. Conversely, obesity related chronic inflammation of the hypothalamus can disturb anorexigenic signals and promote abnormal body weight control. The aim of the present study was to compare the global hypothalamic endophenotype in C57/Bl6 mice exposed to a high-fat diet or with acute illness mediated by LPS. Ten-week old male C57/Bl6 mice (n=18) were randomly divided into four groups; the control 1 group (n =3) was fed a normal diet whereas the high-fat diet (HFD) group (n =6) was fed a high-fat diet for eight weeks. The control 2 group (n=3) received an intraperitoneal injection of saline whereas the LPS group (n=6) received an intraperitoneal injection of LPS. Mice were sacrificed 18-hr post-injection. Both control 2 and LPS groups were fed a normal diet for eight weeks before the injection. The hypothalamic regions were removed and analysed using a 2D LC-MS methodology. The proteomic analysis profiled 9,235 proteins (q<0.05) across all biological states, of which 522 proteins were found modulated in the HFD group and another 579 in the LPS group. The proteomic profiles demonstrated that the systemic acute inflammation linked with anorexia induced a negative feedback loop of appetite control in the hypothalamus, suggesting an effort to re-establish homeostasis. By contrast, the chronic inflammation associated with obesity initiated a “perpetual cycle” of positive feedback enhancement of appetite regulation further exacerbating positive energy balance.
