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P21 is an inhibitor of the cell cycle [24], [25] and p21 absence in islets had no effects on islet mass and glucose metabolism [24].
Similarly, mice deficient in Skp2, which is responsible for the normal degradation of p27Kip1, present ubiquitous higher levels of p27Kip1, decreased β-cell mass and glucose intolerance, and all these phenotypes are rescued in Skp2/p27Kip1-doubly Skp2/p27Kip1-doubly.
To determine whether inhibition of myostatin signaling in adipose tissue alters adipose tissue mass and glucose metabolism independent of increased skeletal muscle mass, we generated a transgenic mouse line expressing a dominant negative (DN) Acvr2b gene specifically in adipocytes.
HFD was associated with increased body mass and glucose intolerance.
Moreover, changes in these bacteria positively correlated with changes in fat mass and glucose homeostasis.
KO mice also present impaired muscle differentiation, reduced muscle mass and glucose intolerance.
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During pregnancy, levels of prolactin and prolactin receptors elevate in parallel with the increase of β-cell mass and glucose-stimulated insulin secretion to upregulate islet cell function and maintain normal glucose homeostasis (14– 14).
Cyclin D2−/− mice showed decreased postnatal β-cell mass and deregulated glucose homeostasis, glucose intolerance as well as diabetes (Georgia & Bhushan, 2004).
In an animal model, RYGB induces weight loss from reduction in fat mass and fasting glucose improves, as does glucose tolerance.
It was found that glucose mass fraction and glucose to fructose ratio strongly affected the steady shear viscosity of TBV-M and that the viscosity changed with temperature according to the Arrhenius's law in the range of 20 60 °C.
Fermentation performance in mineral medium with 40 g/L glucose is presented in Fig. 2. Fig. 2A B shows results obtained for cell mass formation and glucose consumption.
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