Disruption of Gpr45 causes reduced hypothalamic POMC expression and obesity

Abstract

SZ helped analyze the screen data. XW conceived of and designed the studies, supervised the work, and wrote the manuscript. YW and LX performed the electrophysiology studies. MZ and WJ performed the hyperinsulinemic-euglycemic clamp analysis.

MicroRNA‐188 regulates aging‐associated metabolic phenotype

“…Our findings showed that the aged miR‐188 null mice had an unchanged food intake (Figure g); however, their oxygen (O 2 ) consumption and energy expenditure (EE) were significantly higher compared with those of their WT littermates (Figure h–i), which suggested that the decreased body fat mass of the aged miR‐188 null mice was largely the result of increased energy expenditure. Under a normal environmental temperature, energy expenditure mainly comprises thermogenesis and physiological activities (Cui et al, ). Although their physiological activities were not changed (Figure m,n), the aged miR‐188 null mice had a significantly higher body temperature than their WT littermates (Figure o).…”

“…In the aged miR‐188 null mice and aged adipose tissue‐specific miR‐188 transgenic mice, the food intake was unchanged; however, the oxygen consumption and energy expenditure were significantly increased or decreased compared with those in the corresponding control mice, respectively. Under normal environmental conditions, energy expenditure occurs through physiological activities and thermogenesis (Cui et al, ; Deng et al, ; Wyler, Lord, Lee, Elmquist, & Liu, ). The mice's physiological activities were unchanged; however, the expression of thermogenesis‐related genes increased or decreased significantly in the BAT and iWAT of aged miR‐188 null mice or aged adipose tissue‐specific miR‐188 transgenic mice, respectively.…”

The Vitamin K Epoxide Reductase Vkorc1l1 Promotes Preadipocyte Differentiation in Mice

“…We have identified a Vkorc1l1 mutant through a forward genetic screen for obesity‐related loci in mice . In this report, we show that disruption of Vkorc1l1 leads to defective adipogenesis associated with increased vitamin K 2 in preadipocytes.…”

Efficient genome-wide first-generation phenotypic screening system in mice using the piggyBac transposon

“…Based on the data obtained from our growth retardation screen and previously reported ENU screens (7,8), we estimate that our engineered transposon is 5-fold more potent than ENU in its ability to induce functional mutations (SI Appendix, Table S2). Moreover, we previously conducted a PB insertional recessive screen for obesity (21). We recorded the body weight of all animals in the obesity screen and have now analyzed the original data from the screen for growth retardation.…”

“…A Pilot PB F1 Dominant Screen for Growth Retardation. We have previously used both ES-based knockout technology and the PBbased F3 recessive screening system in mice to study mechanisms underlying body size control (20,21). To evaluate the power of our F1 screening system, we conducted a pilot screen for a growth retardation phenotype, an important phenotype that serves as an indicator of many systematic defects: 2,036 F1 animals were screened before weaning age and compared to their wild-type siblings from the same litter.…”