PMID:2853465

Citation	Sutcliffe, JG and Milner, RJ (1988) Alternative mRNA splicing: the Shaker gene. Trends Genet. 4:297-9
Abstract	No abstract in PubMed
Links	PubMed
Keywords	Animals; Carrier Proteins/genetics; Chromosome Mapping; Drosophila; Potassium Channels; RNA Splicing; Sodium Channels; Xenopus
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
MOUSE:PLIN1		GO:0045598: regulation of fat cell differentiation	ECO:0000315:		P		Figure 3 shows that "Body weight gain of female hTg and mTg mice was similar to WT controls when fed a normal chow diet (ND) (data not shown). In contrast, when female mice were fed a HFD, both hTg and mTg mice gained weight less rapidly than their WT littermates (Fig. 3A, B). Male hTg mice had a very small but significant reduction in body weight gain when fed a HFD compared with WT littermates, whereas mTg did not differ from WT in their weight gain on an HFD. Since both female hTg and mTg mice demonstrated a more robust phenotype compared with male transgenic mice, the data presented throughout this manuscript focused only on female mice. At 30 weeks of age (25 weeks of HFD), both hTg and mTg mice weighed ~20% less than WT controls (Fig. 3A, B). The observed difference in body weight became significant after the animals reached 13 (hTg) and 22 (mTg) weeks of age, respectively. Regardless of diet, food intake was similar between Tg and WT mice and was not a contributing factor to the observed differences in body weight on the HFD (WT 2.28 ± 0.16g vs. 2.09 ± 0.09g, P = 0.55). In spite of their similar food consumption level, fasting serum leptin concentration was significantly lower in HFD-fed hTg mice compared with WT mice (9.83 ± 3.57 vs. 32.85 ± 0.02 ng/ml) (P = 0.003), which is probably explained by smaller adipocyte in hTg mice."	complete CACAO 5601

References

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