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As expected, the Ldlr-3KO mice were obese, extremely hypercholesterolemic (including elevated HDL-cholesterol) and hypertriglyceridemic compared with Ldlr-2KO mice (Table S1, [20]).
Both male and female KO mice were obese, but through different mechanisms.
HP-fed mice were obese and insulin resistant and had altered insulin-induced Akt phosphorylation in skeletal muscle (SkM).
Like ob/ob mice, the ob/obIL6 mice (generated by intercrossing ob/ob and h IL6tg mice) were obese and glucose-intolerant.
It has been observed that most Prox1+/− adult mice were obese compared with their wild-type counterparts [ 3]. Figure 5 shows abnormal lymphatic drainage patterns from the injection site on the base of the tail.
Specifically, by 1 year of age male GLE mice were obese (Pizzi and Barnhart 1976), and the weight gain was greater in low-and moderate-dose than in high-dose GLE mice.
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Mice that lack β1, β2 and β3 adrenergic receptors ('beta-less' mice) are obese, primarily the result of defective SNS-dependent activation of diet-induced thermogenesis because lipolytic responses to fasting were not altered [ 79, 80].
It is known that ERα knock-out (ERαKO) mice are obese and insulin resistant [2].
These data indicate that AC3−/− mice are obese because they eat more and are less active.
Although neither COX1 KO nor COX2 KO mice are obese, COX2+/− KO mice have more adipose tissue than wild-type littermates when fed an obesogenic diet [48].
It is also worth noting that the Ay-Jkn1 mice are obese as a result of inhibiting the MC4R, and the role that this has to play in terms of behavioural reflex assessment of the hindlimb needs further clarification.
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