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Development of dyslipidemia.
Treating wild type mice with the FXR agonist (chenodeoxycholic acid, CDCA) protected against development of dyslipidemia induced by ritonavir.
These results also demonstrate that under a HFD, ctsk deficiency confers a partial resistance to the development of dyslipidemia.
Further, our results demonstrate that under a HFD, ctsk deficiency confers a partial resistance to the development of dyslipidemia.
Thus, not only activation of FXR with CDCA protects against development of dyslipidemia caused by ritonavir, but feeding ritonavir to FXR−/− mice resulted in an exacerbation of biochemical derangements caused by the HIV PI in wild type mice.
Adult ctsk−/− mice, which do not display overt phenotypic alterations when fed a normal diet, displayed a partial resistance to weight gain and to development of dyslipidemia when challenged with a HFD.
Similar(36)
Although diet certainly contributes to the development of dyslipidemias, genetic factors are also involved.
Therefore, it was possible to study the development and evolution of dyslipidemia prospectively in this study.
Simultaneous exposure to various POPs in the general population may contribute to development of obesity, dyslipidemia, and insulin resistance, common precursors of type 2 diabetes and cardiovascular diseases.
In conclusion, low dose POPs may be involved in the development of obesity, dyslipidemia, and insulin resistance, although different POPs may relate to different metabolic traits.
These factors may contribute to the development of hypertension, dyslipidemia, and hyperglycemia, as well as cancer.
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