Abnormal insulin and beta-adrenergic modulation of lipoprotein liipase during refeeding after prolonged fasting in the Zucker rat

Diabetologia. 2000 Jul;43(7):866-74. doi: 10.1007/s001250051463.

Abstract

Aims/hypothesis: To characterise the response of tissue lipoprotein lipase to refeeding after prolonged (24 h) fasting in lean and obese Zucker rats, and to verify whether lipoprotein lipase in obese rats is resistant to the short-term action of insulin and escapes modulation by the beta-adrenergic pathway.

Methods: Lean Fa/? and obese fa/fa male Zucker rats fasted for 24 h and refed at will. Lipoprotein lipase activity in adipose and muscle tissues was assessed in the freely fed and fasted states and at various times during refeeding, with or without beta-adrenergic blockade (propranolol).

Results: The 24 h fast erased the phenotype-related differences in insulinaemia and adipose lipoprotein lipase activity present in freely fed rats. Adipose lipoprotein lipase increased twofold in obese rats 1 h after refeeding, whereas no change occurred at that time in lean rats. Activity remained at that level for at least 6 h after refeeding in obese rats, whereas in lean animals it was increased fivefold after 6 h of refeeding. In muscle of obese rats, lipoprotein lipase decreased in response to refeeding, but paradoxically increased twofold in lean animals. Giving propranolol to lean rats before refeeding abolished the atypical response of muscle lipoprotein lipase to food intake and restored the early (1 h after refeeding) increase in adipose lipoprotein lipase but had no effect in obese rats.

Conclusion/interpretation: Refeeding after prolonged fasting activates the P-adrenergic pathway in lean rats, which transiently counteracts insulin-mediated modulation of lipoprotein lipase. The P-adrenergic pathway is not activated by refeeding in adipose tissue and muscle of the obese Zucker rat. In the obese Zucker rat, the early modulation of adipose lipoprotein lipase activity is abnormal upon refeeding after prolonged fasting, suggesting short-term resistance to the action of insulin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / enzymology
  • Adrenergic beta-Antagonists / pharmacology*
  • Animals
  • Body Weight
  • Eating / physiology*
  • Fasting / physiology*
  • Food Deprivation
  • Kinetics
  • Lipoprotein Lipase / metabolism*
  • Male
  • Muscle, Skeletal / enzymology
  • Obesity / genetics
  • Obesity / physiopathology*
  • Propranolol / pharmacology*
  • Rats
  • Rats, Zucker
  • Thinness

Substances

  • Adrenergic beta-Antagonists
  • Propranolol
  • Lipoprotein Lipase