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While the FCTC may not be the appropriate model for diet and obesity, the paper makes a special case for the development of binding international standards in select areas of diet and nutrition.
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We investigated the effects of 7 diets from a single manufacturer containing 11 58 en% protein (casein), 0 81 en% carbohydrates (CHO; sucrose, maltrodextrin-10 and corn starch), and 8 42 en% fat (triheptanoin, olive oil or cocoa butter) in C57BL/6 J mice, a good model for diet-induced obesity and fatty liver.
MTCRII may thus provide the basis for an intermediate risk assessment model for diet- or lifestyle-related genotoxic/nongenotoxic chemical combinations, relevant to colonic health.
Our results suggest that BioF1B Golden Syrian hamsters are a potential model for diet-induced metabolic syndrome with associated non-alcoholic fatty liver disease.
To determine how successful our approach was in identifying plausible novel candidates, we compared differentially expressed genes from our mouse model for diet-induced diabetes with previously reported single nucleotide polymorphisms (SNPs) associated with type 2 diabetes in humans.
In the present study we therefore studied myocardial function and perfusion under baseline and pharmacological-induced hyperaemic conditions in a rat model for diet-induced glucose intolerance using contrast echocardiography.
Although zebrafish larvae have been used in genetic and chemical screening experiments to identify novel genes involved in the regulation of energy homeostasis and potential therapeutic targets to treat obesity [ 13, 23], it remains unclear whether zebrafish can be used as a model for diet-induced obesity (DIO), similar to that observed in mammals.
Another limitation is that it was not possible to adjust models for diet, as such data were not collected.
In addition to age, sex, BMI and WHR, we adjusted our models for diet (total calorie and macronutrient intakes), physical activity and socioeconomic status at 21 years.
Daily Growth Coefficient (DGC) was studied using a model accounting for diet as a fixed effect and tank, sire, dam, sire*diet and dam*diet as random effects, using SAS-GLM.
Our findings further demonstrate the potential utility of this animal model for studying diet-induced metabolic dysregulation.
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