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The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 1 302-307
Copyright © 2002 by The Endocrine Society


Other Original Articles

Metabolic Adaptation to Feeding and Fasting during Lactation in Humans

Stelios Tigas, Agneta Sunehag and Morey W. Haymond

Department of Pediatrics, Children’s Nutrition Research Center, United States Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston, Texas 77030

Address all correspondence and requests for reprints to: M. W. Haymond, M.D., CNRC, 1100 Bates Street, Houston, Texas 77030-2600. E-mail: mhaymond{at}bcm.tmc.edu

The aim of these studies was to determine the metabolic adaptation to fasting and feeding during lactation. Normal lactating (L) and nonlactating (NL) women (n = 6 each) were studied using infusions of [U-13C]glucose and [2-13C]glycerol during: 1) a 24-h fast, and 2) ingestion of Sustacal (protocol 1). In addition, 8 L and 6 NL women were studied during infusion of [6,6-2H2]glucose and ingestion of a glucose meal containing [1-13C]glucose (protocol 2). Protocol 1: Glucose production rate (GPR) during fasting was 33% higher in the L women (12.5 ± 1.0 vs. 9.4 ± 0.5 µmol·kg-1·min-1; P < 0.03). Fractional gluconeogenesis (GNG), GNG rate, glucose, lactate, ß- hydroxybutyrate, FFA, insulin, and C-peptide were similar in both groups during feeding and fasting, but glycogenolysis was 50% higher in fasting L women. Protocol 2: Although GPR was slightly increased in the L group (L, 1.8 ± 0.2 µmol·kg-1·min-1; NL, 1.2 ± 0.2 µmol·kg-1·min-1; P < 0.04), no other differences were observed in splanchnic and systemic metabolism of ingested glucose between L and NL women. Insulin concentrations were lower in L women compared with controls (L, 15 ± 3 µU/ml; NL, 28 ± 6 µU/ml; P = 0.05). In conclusion, the increased glucose demands of lactation are met by increased GPR as a result of increased glycogenolysis but not GNG or by increased use of FFA. During feeding, lactating women handle oral carbohydrates normally but have increased insulin sensitivity.

This project was supported by grants from NIH (RO1 DK 55478 and HD37857), U.S. Department of Agriculture (USDA) Cooperative Agreement no. 58-6250-6-001, and the Baylor GCRC (1-RR-00188).

This work is a publication of the USDA/Agricultural Research Service, CNRC, Department of Pediatrics, Baylor College of Medicine, Houston, TX. The contents of this publication do not necessarily reflect the views of policies of the USDA, nor does mention of trade names, commercial products, or organizations imply endorsement from the U.S. Government.

Abbreviations: CNRC, Children’s Nutrition Research Center; GCMS, gas chromatography-mass spectrometry; GCRC, General Clinical Research Center; GNG, gluconeogenesis; GPR, glucose production rate; L, lactating; NL, nonlactating; Ra, rate of appearance; USDA, U.S. Department of Agriculture; VCO2, rate of CO2 expired.




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