Adaptation to increasing loads of total parenteral nutrition: Metabolic, endocrine, and insulin receptor responses☆

Abstract 

The metabolic, hormonal, and insulin receptor responses to the initiation, maintained infusion, and cessation of a total parenteral nutrient solution were assessed in 5 adult patients with gastrointestinal disorders as part of a program of home total parenteral nutrition. Three phases were studied: phase 1, continuous infusion; phase 2, 17 h of infusion; and phase 3, the 12-h night-time schedule. In the first 2 phases, all subjects responded well. Blood glucose was in the range of 100–130 mg/dl; nitrogen balance, positive; and weight gain, progressive. The major response to the abrupt initiation of the infusion was brisk insulin secretion. Tapering resulted in a fall of glucose to fasting levels and a rapid decline in insulin. No significant changes in glucagon, cortisol, or growth hormone were noted with initiation or cessation. During phase 3, 4 of the 5 patients had patterns similar to phase 2, although plasma glucose and insulin responses were higher. There was no post-infusion hypoglycemia, and the glycemic responses to glucagon 11 h postinfusion suggested preservation of glycogen stores. One subject tolerated the infusion in phases 1 and 2, but not in phase 3. While his insulin responses were essentially equal to the other 4, marked hyperglycemic, hyperglucagonemia, and higher growth hormone and cortisol levels were noted. During phase 3 total insulin binding to circulating monocytes was significantly diminished in all patients. This decrease was predominantly a function of a decrease in high-affinity receptors and may reflect receptor “downregulation” by the hyper-insulinemia which developed with each infusion. Thus, adaptation to the initiation, infusion, and cessation of nutrients during home total parenteral nutrition is characterized by abrupt alterations in insulin secretion without apparent changes in counterregulatory hormones. The responses to insulin may be modulated by regulatory changes in insulin receptors which could predispose some patients to carbohydrate intolerance while protecting others from postinfusion hypoglycemia.

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