Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction

Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations...

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Veröffentlicht in:Obesity (Silver Spring, Md.) Md.), 2009-09, Vol.17 (9), p.1702-1709
Hauptverfasser: Shi, Haifei, Akunuru, Shailaja, Bierman, John C, Hodge, Karen M, Mitchell, M. Chrissy, Foster, Michelle T, Seeley, Randy J, Reizes, Ofer
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container_end_page 1709
container_issue 9
container_start_page 1702
container_title Obesity (Silver Spring, Md.)
container_volume 17
creator Shi, Haifei
Akunuru, Shailaja
Bierman, John C
Hodge, Karen M
Mitchell, M. Chrissy
Foster, Michelle T
Seeley, Randy J
Reizes, Ofer
description Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.
doi_str_mv 10.1038/oby.2009.106
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HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. 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Chrissy</creatorcontrib><creatorcontrib>Foster, Michelle T</creatorcontrib><creatorcontrib>Seeley, Randy J</creatorcontrib><creatorcontrib>Reizes, Ofer</creatorcontrib><title>Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obesity (Silver Spring)</addtitle><description>Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high‐fat (HF) diet–induced obese (DIO) mice were switched to a low‐fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF‐chow), but retained a greater amount of adiposity than chow‐fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF‐chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF‐chow mice. Leptin administration was used to test whether reduced leptin level of HF‐chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF‐HF mice had lower mRNA levels of β3 adrenergic receptor (β3‐AR) in epididymal WAT (EWAT) compared to chow‐fed mice, and diet change led to an increase in the WAT β3‐AR mRNA levels that were similar to the levels of chow‐fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF‐HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF‐chow mice were resistant to further fat loss due to leptin insufficiency. 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subjects Adipocytes
adipose tissue
Adipose Tissue, Brown - metabolism
Adipose Tissue, Brown - pathology
Adipose Tissue, Brown - physiopathology
Adipose Tissue, White - metabolism
Adipose Tissue, White - pathology
Adipose Tissue, White - physiopathology
Adiposity
animal models
Animals
Blood Glucose - metabolism
Body fat
body weight
Cell Size
Diet
Diet, Fat-Restricted
diet-related diseases
Dietary Fats - administration & dosage
Digitization
Disease Models, Animal
Eating
Fatty Liver - etiology
Fatty Liver - metabolism
Fatty Liver - physiopathology
Feeding Behavior
Glucose
high fat diet
Histology
human diseases
Inflammation - etiology
Inflammation - metabolism
Inflammation - physiopathology
Insulin - blood
Insulin resistance
leptin
Leptin - blood
Leptin - deficiency
low fat diet
Macrophages - metabolism
Male
Metabolism
Mice
Mice, Inbred C57BL
Obesity
Obesity - diet therapy
Obesity - etiology
Obesity - metabolism
Obesity - physiopathology
Physiology
quantitative analysis
Receptors, Adrenergic, beta-3 - genetics
RNA, Messenger - metabolism
Time Factors
Weight control
Weight Loss
title Diet-induced Obese Mice Are Leptin Insufficient After Weight Reduction
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