DOI: 10.1530/JOE-16-0031
Journal of Endocrinology
229:2
http://joe.endocrinology-journals.org © 2016 Society for Endocrinology
Printed in Great Britain
Published by Bioscientifica Ltd.
145–157
Abstract
Mammals meet the increased nutritional demands of lactation through a combination
of increased feed intake and a collection of adaptations known as adaptive metabolism
(e.g., glucose sparing via insulin resistance, mobilization of endogenous reserves, and
increased metabolic effciency via reduced thyroid hormones). In the modern dairy
cow, adaptive metabolism predominates over increased feed intake at the onset of
lactation and develops concurrently with a reduction in plasma leptin. To address the
role of leptin in the adaptive metabolism of early lactation, we asked which adaptations
could be countered by a constant 96-h intravenous infusion of human leptin (hLeptin)
starting on day 8 of lactation. Compared to saline infusion (Control), hLeptin did not
alter energy intake or milk energy output but caused a modest increase in body weight
loss. hLeptin reduced plasma glucose by 9% and hepatic glycogen content by 73%,
and these effects were associated with a 17% increase in glucose disposal during an
insulin tolerance test. hLeptin attenuated the accumulation of triglyceride in the liver
by 28% in the absence of effects on plasma levels of the anti-lipolytic hormone insulin
or plasma levels of free fatty acids, a marker of lipid mobilization from adipose tissue.
Finally, hLeptin increased the plasma concentrations of T
4
and T
3
by nearly 50% without
affecting other neurally regulated hormones (i.e., cortisol and luteinizing hormone
(LH)). Overall these data implicate the periparturient reduction in plasma leptin as one
of the signals promoting conservation of glucose and energy at the onset of lactation in
the energy-defcient dairy cow.
R A EHRHARDT and others Leptin action in early lactating
dairy cows
Increased plasma leptin attenuates
adaptive metabolism in early
lactating dairy cows
Richard A Ehrhardt
1
, Andreas Foskolos
2
, Sarah L Giesy
3
, Stephanie R Wesolowski
4
,
Christopher S Krumm
3
, W Ronald Butler
3
, Susan M Quirk
3
, Matthew R Waldron
3
and
Yves R Boisclair
3
1
Departments of Animal Science and Large Animal Clinical Sciences, Michigan State University,
East Lansing, Michigan, USA
2
Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, UK
3
Department of Animal Science, Cornell University, Ithaca, New York, USA
4
University of Colorado School of Medicine, Aurora, Colorado, USA
Journal of Endocrinology
(2016) 229, 145–157
Research
Key Words
f glucose metabolism
f lipid metabolism
f liver
f thyroid hormone
Correspondence
should be addressed
to Y Boisclair
Email
yrb1@cornell.edu
Introduction
In most mammals, the nutrient demands of lactation
are met by a combination of increased voluntary feed
intake and adaptive metabolism (Vernon et al. 2002).
Adaptive metabolism refers to processes preserving
metabolic homeostasis during periods of energy
insuffciency and includes mobilization of endogenous
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