How murine models of human disease and immunity are influenced by housing temperature and mild thermal stress

James, Caitlin M.; Olejniczak, Scott H.; Repasky, Elizabeth A.

doi:10.1080/23328940.2022.2093561

Cited by 5 publications

(2 citation statements)

References 73 publications

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“…Animal facilities are predominantly maintained at "room temperature" (19-22 • C) for the comfort of the human work environment [63,64]. The thermoneutral (TN) zone, or temperature of metabolic homeostasis, for C57BL/6 mice is between 30-32 • C [20].…”

Section: Introductionmentioning

confidence: 99%

“…Notably, TN housing increases adipocyte size in murine inguinal white adipose tissue (iWAT) [68] and causes mouse brown adipose tissue (BAT) to closely resemble human BAT [69]. Such modulation of mouse physiology has allowed TN housing to improve mimicry of many human disease models, including cancer [64,[70][71][72][73], atherosclerosis [21,74], asthma [75], food allergy [76], and liver disease [77]. Specifically, TN housing allows for induction of HFD-induced severe obesity and amplifies severity of obesity-associated sequelae (e.g., glucose dysmetabolism, hepatocellular damage, influenza virus infection pathology) in WT female C57BL/6 mice [20,78].…”

Section: Introductionmentioning

confidence: 99%

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Thermoneutral Housing Enables Studies of Vertical Transmission of Obesogenic Diet-Driven Metabolic Diseases

Wayland,

Doll,

Lawson

et al. 2023

Nutrients

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Vertical transmission of obesity is a critical contributor to the unabated obesity pandemic and the associated surge in metabolic diseases. Existing experimental models insufficiently recapitulate “human-like” obesity phenotypes, limiting the discovery of how severe obesity in pregnancy instructs vertical transmission of obesity. Here, via utility of thermoneutral housing and obesogenic diet feeding coupled to syngeneic mating of WT obese female and lean male mice on a C57BL/6 background, we present a tractable, more “human-like” approach to specifically investigate how maternal obesity contributes to offspring health. Using this model, we found that maternal obesity decreased neonatal survival, increased offspring adiposity, and accelerated offspring predisposition to obesity and metabolic disease. We also show that severe maternal obesity was sufficient to skew offspring microbiome and create a proinflammatory gestational environment that correlated with inflammatory changes in the offspring in utero and adulthood. Analysis of a human birth cohort study of mothers with and without obesity and their infants was consistent with mouse study findings of maternal inflammation and offspring weight gain propensity. Together, our results show that dietary induction of obesity in female mice coupled to thermoneutral housing can be used for future mechanistic interrogations of obesity and metabolic disease in pregnancy and vertical transmission of pathogenic traits.

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Section: Introductionmentioning

confidence: 99%