In this study, subjects were put in a stressful situation and then their leptin levels were taken.
Because wild-type and ob-norm animals differed only in their plasma leptin levels, this result confirms that hyperleptinemia is functionally required for the development of leptin resistance after long-term exposure to a high-fat diet.
This could be due to their low leptin levels (2.5 ng/mL), at which leptin has not been found to exert significant vasodilation in Japanese subjects [ 10].
To test whether the leptin resistance in BBS mice is secondary to obesity, we examined the appetite-suppressing and weight-reducing effects of exogenous mouse leptin in BBS mice that had their circulating leptin levels normalized by calorie restriction.
Although the mechanism for an association with colon carcinogenesis is unknown, it is hypothesized that insulin and leptin resistance may play a role because leptin levels are typically threefold higher in the genetically obese Zucker (fa/fa) rats than in their lean counterparts, because of the leptin receptor defect in these animals [ 39].
Because leptin levels were increased in rats from litters of four pups and astrocytes express leptin receptors (17, 18, 20), we hypothesized that chronic exposure to increased leptin may be involved in the observed glial changes.
Because leptin levels are elevated in obese individuals and excess body weight has been shown to increase breast cancer risk in postmenopausal women, attempts have been made to evaluate whether leptin can promote breast cancer.
However, this may not be the case in early stages of AD, because differences in CSF leptin levels at the early phases of AD progression were not found.
To test whether Dbh −/− mice do not enter torpor upon fasting because of their failure to suppress circulating leptin levels, we bred Dbh −/− mice onto a leptin-deficient (ob/ob) background to produce double knockout (DBL MUT) mice.
Although obese animals and humans frequently have elevated circulating leptin levels, their leptin fails to mediate weight loss, implicating resistance to the action of leptin in obese states.
