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These mice have improved inflammatory profile in adipose tissue, along with improved systemic insulin sensitivity and ameliorated hepatic steatosis (Weisberg et al 2006).
Our prior work has demonstrated that PF4−/− mice have improved ECM survival and reduced plasma cytokines.
Monocyte depleted Plasmodium berghei infected mice have improved survival, and KLF4 is greatly increased in control, but not monocyte depleted mice.
Our results show that Mstn−/− mice have improved glucose metabolism and increased insulin sensitivity on both standard chow and high fat diet.
Fetuin-A knockout mice have improved insulin sensitivity and are resistant to weight gain on a high-fat diet [28], [29].
Our previous studies showed that aged Ghsr −/− mice have improved insulin sensitivity [ 34].
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While there is still some debate as to whether plaques are a cause or a symptom of Alzheimer's, the experiment found that the treated mice had improved memory, as measured by three different tests, compared with untreated ones.
Pmch−/−; Scd1−/− double-knockout mice had improved glucose tolerance relative to control mice.
CD80−/− mice had improved survival after CLP when compared to WT or CD86−/− mice.
CD28−/− mice had improved overall and median survival compared to WT mice after CLP (Figure 1A).
IPGTT showed that GLP-1/hIgG2-treated MDSD mice had improved glucose tolerance (Figure 7D).
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