Discovering The Developmental Origins of Obesity

The Polish Academy of Sciences in Olsztyn, Poland


Genetic variation in brown fat activity and body weight regulation in mice: Lessons for human studies

Leslie P. Kozak
Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, ul. Tuwima 10, Olsztyn 10-748, Poland

Diet induced obesity, Ucp1−/− mice, Brown adipose tissue and thermogenesis, aP2-Ucp1 transgenic mice, Allelic variation and Ucp1 expression, Muscle and diet-induced thermogenesis

The recent characterization of brown fat in humans has generated much excitement on the possibility that increased energy expenditure by heat production by this tissue will be able to reduce obesity. This expectation has largely been stimulated by studies with mice that show strong associations between increased brown fat activity and reductions in obesity and insulin resistance. Research in the mouse has been largely based upon the induction or suppression of brown fat andmitochondrial uncoupling protein by genetic methods.


Inherent Plasticity of Brown Adipogenesis in White Fat of Mice Allows for Recovery from Effects of Post-Natal Malnutrition

Leslie P. Kozak1, Robert A. Koza2, Rea Anunciado-Koza2, Tamra Mendoza2, Susan Newman2

1 Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, Olsztyn, Poland,
2 Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States of America

Interscapular brown adipose tissue (iBAT) is formed during fetal development and stable for the life span of the mouse. In addition, brown adipocytes also appear in white fat depots (wBAT) between 10 and 21 days of age in mice maintained at a room temperature of 23uC. However, this expression is transient. By 60 days of age the brown adipocytes have disappeared, but they can re-emerge if the adult mouse is exposed to the cold (5uC) or treated with b3-adrenergic agonists. Since the number of brown adipocytes that can be induced in white fat influences the capacity of the mouse to resist the obese state, we determined the effects of the nutritional conditions on post-natal development (birth to 21 days) of wBAT and its longterm effects on diet-induced obesity (DIO).


The effects of early under-nutrition on the development of wBAT and obesity

Leslie P. Kozak
Institute of Animal Reproduction and Food Research; Polish Academy of Sciences; Olsztyn, Poland

Keywords: perinatal under-nutrition, brown adipocyte differentiation in white fat, diet-induced obesity, microarray analysis of gene expression, mitochondrial uncoupling protein1

Correspondence to: Leslie P. Kozak;
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Heat from calcium cycling melts fat

Leslie P Kozak & Martin E Young

A new study in mice shows that sarcolipin, a small, regulatory protein of the intracellular calcium pump (SERCA) in skeletal muscle, is part of a nonshivering thermogenic mechanism for regulating both core body temperature and energy balance (pages 1575–1579).

Leslie P. Kozak is at the Institute of Animal Reproduction and Food Research of the Polish Academy of Science, Olsztyn, Poland.
Martin E. Young is in the Division of Cardiovascular Diseases, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.

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Inactivation of the Mitochondrial Carrier SLC25A25 (ATP-Mg2+/Pi Transporter) Reduces Physical Endurance and Metabolic Efficiency in Mice

Rea P. Anunciado-Koza1, Jingying Zhang, Jozef Ukropec2, Sudip Bajpeyi, Robert A. Koza, Richard C. Rogers, William T. Cefalu, Randall L. Mynatt, and Leslie P. Kozak3

From the Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808

An ATP-Mg2+/Pi inner mitochondrial membrane solute transporter (SLC25A25), which is induced during adaptation to cold stress in the skeletal muscle of mice with defective UCP1/brown adipose tissue thermogenesis, has been evaluated for its role in metabolic efficiency. SLC25A25 is thought to control ATP homeostasis by functioning as a Ca2+-regulated shuttle of ATP-Mg2+ and Pi across the inner mitochondrial membrane. Mice with an inactivated Slc25a25 gene have reduced metabolic efficiency as evidenced by enhanced resistance to diet-induced obesity and impaired exercise performance on a treadmill.