Effects of limited food intake on the obese-hyperglycemic syndrome

Abstract

In ob/ob mice a 12-wk period of food restriction led to a reduced rate of somatic growth and a decreased lean body mass, along with small but reliable reductions in systemic immunoreactive insulin levels and evidence of increased insulin sensitivity. However, no effects of limited access to food were noted on the basal hyperglycemia, the elevated percent carcass lipid, or on the significantly higher levels of serum corticoids that occur in obese animals. These data indicate that hyperphagia alone is not responsible for the maintenance of many of the commonly reported characteristics of the obese-hyperglycemic syndrome, but do not exclude the contribution of factors secondary to the quantity of ingested food. Additionally, the present data lend support to recent work suggesting that chronic hyperinsulinemia or an elevated set point of total carcass lipid may be instrumental in the development of this syndrome.

Starvation and Age Effects on Glycoregulation and Hormone Levels of C57BL/6J ob/ob Mice

“…In the present studies we corroborated previous findings (Bailey et al 1977;Dubuc 1976b;Garthwaite et al 1980) by showing that between 3 and 6 months of age the fed and 24-hour fasted glucose levels of ob/ob mice are reduced to the range of lean mice. We could not detect a hormonal basis for these age-related glycemic changes since they occurred in the absence of either elevated insulin or reduced glucogenic hormone production.…”

“…Coincident with weaning (21-28 days of age) fasting hyperglycemia, glucose intolerance, and in vivo insulin 'insensitivity' are first detected (Dubuc and Willis 1979). The metabolic state progressively deteriorates with age and by about 12 weeks of age the most severe diabetes is observed (Bailey, Atkins, Flatt,Best and Matty 1977;Dubuc 1976b;Garthwaite,Martinson, Tseng,Hagen and Menahan 1980). During the next few months fasting glycemia slowly returns to levels within the range of the lean littermates (Bailey et al 1977;Dubuc 1976b;Garthwaite et al 1980).…”

“…The metabolic state progressively deteriorates with age and by about 12 weeks of age the most severe diabetes is observed (Bailey, Atkins, Flatt,Best and Matty 1977;Dubuc 1976b;Garthwaite,Martinson, Tseng,Hagen and Menahan 1980). During the next few months fasting glycemia slowly returns to levels within the range of the lean littermates (Bailey et al 1977;Dubuc 1976b;Garthwaite et al 1980). The factors responsible for these age-related changes of glycoregulation are not yet known, but it does not appear that hyperphagia, the high carbohydrate postweaning diet, or tissue insulin 'insensitivity' will account for the glycemic alterations (Bray and York 1979;Czech, Richardson and Smith 1977;Dubuc l976b;Lin, Romsos and Leveille 1977;Rath and Thenen 1979).…”

Fed and Fasting Thermoregulation in ob/ob Mice

“…The ob/ob mouse maintains a carcass fat content about 3 times greater than that of the lean mouse when its daily food intake is the same [3][4][5][6][7] or when it is placed in situations requiring increased energy expenditure [15,22,23], There appear to be at least three mechanisms which allow these mice to retain greater fat stores. First, fat anabolism contin ues at the expense of both lean body mass and skeletal growth when energy require ments exceed energy availability [17,24].…”

“…Separate groups of ad libitum-fed lean (n = 16) and obese (n = 16) mice served as controls for the effects of daily temperature measurement on body weight gain and body temperature. At the end of the 72-hour observation period these ad libitum-fed mice were sacrificed for determination of carcass composition as described earlier [7], along with separate groups of ad libitum-fed, weight-matched gender controls (n = 8 males, n = 8 females). Mice in the postprandial condi tion had rectal temperatures recorded at the end of the feeding period, but we excluded all values from mice not ingesting a minimum of 0.4 g food.…”