4.8 Article

Evidence for a Non-leptin System that Defends against Weight Gain in Overfeeding

期刊

CELL METABOLISM
卷 28, 期 2, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.cmet.2018.05.029

关键词

-

资金

  1. NIH [HL007343, DK007328, DK101942, DK066525]
  2. Berrie Foundation Obesity Initiative
  3. NY Obesity Nutrition Research Center [DK026687]
  4. Columbia Diabetes Research Center [DK063608]

向作者/读者索取更多资源

Weight is defended so that increases or decreases in body mass elicit responses that favor restoration of one's previous weight. While much is known about the signals that respond to weight loss and the central role that leptin plays, the lack of experimental systems studying the overfed state has meant little is known about pathways defending against weight gain. We developed a system to study this physiology and found that overfed mice defend against increased weight gain with graded anorexia but, unlike weight loss, this response is independent of circulating leptin concentration. In overfed mice that are unresponsive to orexigenic stimuli, adipose tissue is transcriptionally and immunologically distinct from fat of ad libitum-fed obese animals. These findings provide evidence that overfeeding-induced obesity alters adipose tissue and central responses in ways that are distinct from ad libitum obesity and activates a non-leptin system to defend against weight gain.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Endocrinology & Metabolism

The postnatal leptin surge in mice is variable in both time and intensity and reflects nutritional status

Alicja A. Skowronski, Evan D. Shaulson, Rudolph L. Leibel, Charles A. LeDuc

Summary: In mice, the postnatal leptin surge within the first 4 weeks of life is significantly influenced by nutritional status. Mice raised in small litters become fatter and have a larger and earlier leptin surge, while those raised in large litters have delayed and reduced surges. Maternal HFD feeding during the perinatal period also augments the leptin surge in pups.

INTERNATIONAL JOURNAL OF OBESITY (2022)

Article Biology

Adipsin promotes bone marrow adiposity by priming mesenchymal stem cells

Nicole Aaron, Michael J. Kraakman, Qiuzhong Zhou, Qiongming Liu, Samantha Costa, Jing Yang, Longhua Liu, Lexiang Yu, Liheng Wang, Ying He, Lihong Fan, Hiroyuki Hirakawa, Lei Ding, James Lo, Weidong Wang, Baohong Zhao, Edward Guo, Lei Sun, Cliff J. Rosen, Li Qiang

Summary: Adipsin is the most upregulated adipokine during MAT expansion in mice and humans in a PPAR gamma acetylation-dependent manner. Genetic ablation of Adipsin in mice specifically inhibited MAT expansion but not peripheral adipose depots, and improved bone mass during calorie restriction, thiazolidinedione treatment, and aging. The effects were mediated through its downstream effector, complement component C3, to prime common progenitor cells toward adipogenesis rather than osteoblastogenesis through inhibiting Wnt/beta-catenin signaling.
Article Genetics & Heredity

Bi-allelic PAGR1 variants are associated with microcephaly and a severe neurodevelopmental disorder: Genetic evidence from two families

Hagit Daum, Mythily Ganapathi, Yoel Hirsch, Emily L. Griffin, Charles A. LeDuc, Jacob Hagen, Simcha Yagel, Vardiella Meiner, Wendy K. Chung, Hagar Mor-Shaked

Summary: Exome and genome sequencing were used to identify the genetic cause of a severe neurodevelopmental disorder in two unrelated Ashkenazi Jewish families with three affected individuals. A rare homozygous variant in the PAGR1 gene was identified, suggesting its association with a novel autosomal recessive syndromic neurodevelopmental disorder. This gene encodes a component of the histone methyltransferase MLL2/MLL3 complex and may play a role in the DNA damage response pathway.

AMERICAN JOURNAL OF MEDICAL GENETICS PART A (2022)

Review Biochemistry & Molecular Biology

Stem Cell-Derived β Cells: A Versatile Research Platform to Interrogate the Genetic Basis of β Cell Dysfunction

Alberto Bartolome

Summary: This article reviews different models to study the genetic basis of beta cell dysfunction, focusing on the recent advances made possible by stem cell applications in the field of diabetes research.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

Article Medicine, Research & Experimental

Notch-mediated Ephrin signaling disrupts islet architecture and β cell function

Alberto Bartolome, Nina Suda, Junjie Yu, Changyu Zhu, Jinsook Son, Hongxu Ding, Andrea Califano, Domenico Accili, Utpal B. Pajvani

Summary: This study suggests that Notch/Ephrin signaling can permanently alter islet architecture during a morphogenetic window in early life, leading to beta cell dysfunction and progression of type 2 diabetes (T2D).

JCI INSIGHT (2022)

Review Biochemistry & Molecular Biology

MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms

Jiani Liang, Margot Chirikjian, Utpal B. Pajvani, Alberto Bartolome

Summary: The expression of MafA, a key transcription factor, is decreased in type 2 diabetes, leading to beta-cell dysfunction. Understanding the regulatory factors of MafA expression may help identify potential therapeutic targets for improving beta-cell function.

BIOMOLECULES (2022)

Article Endocrinology & Metabolism

An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak β-Cell Mass Acquisition

Alberto Bartolome, Yann Ravussin, Junjie Yu, Anthony W. Ferrante, Utpal B. Pajvani

Summary: This study reveals the mechanism of rapid and robust beta-cell hyperplasia in a mouse model of overfeeding-induced obesity. It identifies Sin3a as a novel transcriptional regulator of beta-cell mass adaptation and demonstrates the importance of Sin3a in the acquisition of postnatal beta-cell mass. Overall, the findings provide insights into the regulatory pathway of beta-cell proliferation and validate the overfeeding-induced obesity model as a useful tool for studying beta-cell adaptation.

DIABETES (2022)

Article Endocrinology & Metabolism

Interindividual variability of human thermoregulation: Toward personalized ergonomics of the indoor thermal environment

Dolaana Khovalyg, Yann Ravussin

Summary: This study illustrates the significant interindividual differences in energy expenditure under normal living conditions and highlights the need for personalized thermal conditioning. The findings suggest that individual metabolic rates vary greatly during typical everyday activities, emphasizing the importance of personalized climate control.

OBESITY (2022)

Article Nutrition & Dietetics

Sucrose dampens caffeine-induced blood pressure elevations - A randomized crossover pilot study in healthy, non-obese men

Yann Ravussin, Jean-Pierre Montani, Erik Konrad Grasser

Summary: This study found that in young, non-obese men, a caffeinated and sucrose-sweetened beverage at concentrations similar to classical commercial Cola products exhibited distinct hemodynamic actions. The presence of sucrose dampened caffeine-induced blood pressure elevations, but increased cardiac work.

FRONTIERS IN NUTRITION (2022)

Article Medicine, Research & Experimental

Notch-mediated hepatocyte MCP-1 secretion causes liver fibrosis

Jinku Kang, Jorge Postigo-Fernandez, KyeongJin Kim, Changyu Zhu, Junjie Yu, Marica Meroni, Brent Mayfield, Alberto Bartolome, Dianne H. Dapito, Anthony W. Ferrante, Paola Dongiovanni, Luca Valenti, Remi J. Creusot, Utpal B. Pajvani

Summary: Patients with nonalcoholic steatohepatitis (NASH) have increased expression of liver monocyte chemoattractant protein-1 (MCP-1), which is mainly produced by hepatocytes. Increased MCP-1 expression leads to the infiltration of monocyte-derived macrophages (MoMF) in the liver and the development of liver fibrosis. Activation of the Notch signaling pathway in hepatocytes is closely related to the upregulation of MCP-1 expression in NASH. Inhibition of MCP-1 or the CCR2 receptor can ameliorate liver MoMF infiltration and fibrosis in NASH.

JCI INSIGHT (2023)

Editorial Material Biochemistry & Molecular Biology

The Pancreatic Beta Cell: Editorial

Alberto Bartolome

BIOMOLECULES (2023)

Article Clinical Neurology

Deletion of the Circadian Clock Gene Per2 in the Whole Body, but Not in Neurons or Astroglia, Affects Sleep in Response to Sleep Deprivation

Katrin S. Wendrich, Hamid Azimi, Jurgen A. Ripperger, Yann Ravussin, Gregor Rainer, Urs Albrecht

Summary: The sleep-wake cycle is regulated by the circadian clock and the sleep homeostat. It is not completely understood how these two systems interact. Evidence suggests that the clock gene Per2 may be involved in the sleep homeostatic process. Neurons and astroglial cells in the brain depend on each other metabolically and play a role in sleep regulation. The study found that mice lacking Per2 in all body cells displayed earlier sleep onset after sleep deprivation, while mice lacking Per2 in neurons or astroglial cells were normal in this regard. Systemic Per2 expression seems to be important for the sleep architecture, while neuronal and astroglial Per2 weakly affects sleep amount. The results indicate that Per2 contributes to the timing of the sleep response by delaying sleep onset after sleep deprivation and attenuating the early night rebound response.

CLOCKS & SLEEP (2023)

Article Medicine, Research & Experimental

Hepatic FoxOs link insulin signaling with plasma lipoprotein metabolism through an apolipoprotein M/sphingosine-1-phosphate pathway

Maria Concepcion Izquierdo, Niroshan Shanmugarajah, Samuel X. Lee, Michael J. Kraakman, Marit Westerterp, Takumi Kitamoto, Michael Harris, Joshua R. Cook, Galina A. Gusarova, Kendra Zhong, Elijah Marbuary, Insug O-Sullivan, Nikolaus Rasmus, Stefania Camastra, Terry G. Unterman, Ele Ferrannini, Barry E. Hurwitz, Rebecca A. Haeusler

Summary: This study found that insulin resistance is associated with decreased HDL-associated S1P. Hepatic FoxO transcription factors are regulators of the ApoM/S1P pathway.

JOURNAL OF CLINICAL INVESTIGATION (2022)

暂无数据