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To investigate whether the response of skin γδ T cells in obese mice can be restored by removal from their environment, we isolated epidermal sheets from 10- to 14-week old obese BKS db/db mice and lean db/+ controls and stimulated the skin-resident T cells in vitro with anti-CD3ε antibody.
Obese diabetic mice and lean control animals were exposed to shaking stress.
Expression of total SGLT-1 protein was comparable in both ob/ob mice and lean mice (0.93±0.15 and 0.83±0.16, respectively).
In one mouse model, major differences were observed in the proportion of the different bacterial phyla in genetically obese mice and lean mice.
In agreement with this potential mechanism, germ-free mice and lean individuals also exhibit increased fatty acid oxidation and decreased lipogenesis (Backhed et al. 2007).
In the first series, the effects of acute exercise on blood glucose, insulin, non-esterified fatty acids (NEFA), and CORT levels in db/db mice and lean littermates were determined.
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Intermittent hypoxia resulted in insulin resistance in both genetically obese (25) and lean (7) mice.
In some experiments, the effect of the CB2 antagonist AM-630 (Tocris, France) was evaluated in 6-week-old obese male mice (ob/ob) and lean counterparts (ob+/ob).
C57BL/6J ob/ob mice, C57BL/6J+/? lean mice and A/J mice were given injections of 10 mg/kg of morphine or an equal volume of saline, and then blood was sampled by retroorbital sinus puncture.
We investigated the effects of leptin deficiency on muscle mass and bone architecture in obese, leptin-deficient (ob/ob) mice, and in lean controls.
In an attempt to modify stress hyperglycemia in this animal, we administered either a 5 mg/kg dose of the benzodiazepine alprazolam or vehicle (propylene glycol) intraperitoneally to both obese mice and their lean littermates prior to a rest and a stress period.
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