The characteristics of genetically obese mutants

Effect of Environmental Temperature on Dietary Obesity in Osborne-Mendel Rats

“…The in vitro lipolytic effect of norepinephrine which is observed in the NL-fed rat was entirely eliminated in the HL-fed rat at 28 °C. Such lack of stimulation has pre viously been observed in genetically obese Zucker rats [11] or in the ob/ob mice [2] and has been attributed to either hyperinsulinism or to a loss of thyroid hormone stimula tion [21], In this work, association between hyperinsulincmia (a twofold increase) and HL diet-induced obesity was observed at 28 °C but not at 5 °C (results not seen).…”

Considerations on Genetic and Environmental Factors That Contribute to Resistance or Sensitivity of Mammals Including Humans to Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds

“…It has to be experimentally confirmed if these C57 BL/KsJ-db/db mice and other diabetic mammals are relatively more resistant to shortterm toxicity of TCDD and related chemicals than would be predicted from their high total body fat content (Table 2) because their regulatory pathways of endocrine and metabolic processes are already disturbed. However, it is also known that the C57BL/Ks mice possess the Ah b−1 receptor (Poland et al, 1994) which has a high Festing (1978Festing ( , 1979Festing ( , 1989, York (1979), Herberg (1988), Natori and Kawano (1993), and Herberg and Leiter (1994). binding affinity (e.g., low K d value) to TCDD. From the genetic background it is very likely that the C57BL/Ks-db/db mice are also carrying the Ah b−1 receptor.…”

“…In most specific-pathogen-free colonies, normally untreated diabetic mice will survive for 3 to 4 weeks after the first detection of glycosuria (Leiter, 1993a). Festing (1978Festing ( , 1979, Gad (1992), York (1979), Herberg and Coleman (1977), Herberg (1988), Friedman and Leibel (1992), and Siracusa (1994). a A.d., autosomal dominant; A.r., autosomal recessive.…”

“…Fenton and Chase (1951) reported that male obese yellow (A y /a) mice until 6 months of age and of 50.7 g body wt Note. Source: Adapted with modification from Festing (1978Festing ( , 1978, York (1979), Herberg and Coleman (1977), and Herberg (1988).…”

Energy metabolism in genetically fat and lean birds and mammals

“…The former is accepted as one of the components of all genetic obesities in rodents (York, 1979) although it may not be the primary cause of obesity; the role of energy expenditure has led to more debate (e.g. The most likely causes of genetic obesity are therefore hyperphagia and reduced energy expenditure.…”