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Our lab focuses on the biology of adipose (fat) cells and tissue. Adipose tissue is a highly dynamic and plastic organ, regulating many aspects of whole-body physiology. In addition to its crucial role in maintaining energy levels, adipose tissue regulates body weight, body temperature, blood pressure, insulin sensitivity and serves as a hub for immune responses. Depots of adipose tissue are distributed throughout the body, including underneath the skin, around internal organs, within bones and surrounding large blood vessels, serving specialized functions in each of these locations.
Adipose tissues are defined by the presence of specialized lipid-handling cells called adipocytes. Mammals have two main subtypes of adipocytes, white and brown. White adipocytes are specialized for energy storage and release in response to systemic demand. By contrast, brown adipocytes expend chemical energy (lipid, sugars) in the form of heat to protect animals against hypothermia during cold exposure. Brown fat-like cells, called beige adipocytes, can also be induced to develop within WAT depots in response to various stimuli, thereby augmenting thermogenic capacity.
Adipose tissues are also central players in the development and health consequences of obesity, which has reached epidemic proportions in the US and many parts of the world. Obesity is a leading cause or contributor to an expanding array of diseases such as type 2 diabetes, heart disease, stroke, arthritis, and many types of cancer. In some people, persistent weight gain overburdens the capacity of adipose tissue to safely sequester the excess nutritional energy. In these cases, the adipose tissue becomes inflamed and fibrotic, leading to ectopic deposition of lipid in liver and other tissues. This obesity-induced impairment of adipose tissue function is a primary driver of insulin resistance (pre-diabetes), fatty liver and other metabolic complications, which can eventually progress to type 2 diabetes.
Our lab is investigating mechanisms that control the development and remodeling of adipose tissue in response to external stimuli, such as cold exposure, obesity, and certain diets. In the setting of obesity, promoting adipocyte hyperplasia via the differentiation of resident progenitor cells into new fat cells is associated with improved metabolic health. Furthermore, promoting brown and beige fat cell development and function can protect against obesity and metabolic diseases.
Our projects are divided into two main areas:
(1) Brown fat biology and therapeutic potential.
Brown and beige fat can counteract obesity by expending excess nutritional energy. Increased brown adipose tissue function also promotes a healthy metabolic phenotype by burning toxic metabolites such as fatty acids, glucose, and branched chain amino acids, thereby preventing their accumulation in many organs. In humans, the amount of brown fat tissue is inversely correlated with body mass index, suggesting a potential role for brown fat in regulating body weight. Furthermore, there is great hope that brown fat-targeted therapies can be developed for obesity, fatty liver and diabetes.
Our lab is focused on identifying and understanding the mechanisms that regulate brown fat cell development and function. We are also interested in determining non-canonical functions for brown and beige fat cells in metabolic regulation.
(2) Adipose tissue remodeling responses
Adipose tissue undergoes dynamic metabolic and structural remodeling in response to various stimuli. For example, during cycles of fasting and feeding, adipocytes dramatically alter their metabolic program to accommodate the energetic needs of the organism. Upon chronic cold exposure, white adipose tissue undergoes dramatic remodeling, involving the development of thermogenic beige fat cells, recruitment of blood vessels and increased arborization of nerve fibers. During weight gain, adipose tissue can expand through metabolically beneficial adipocyte hyperplasia and/or via maladaptive adipocyte hypertrophy. In aging, adipose tissue undergoes pronounced fibrotic changes and brown fat activity is reduced.
Our lab is focused on determining the pathways that control these adipose tissue responses. We are focusing on the role of several recently identified mesenchymal cell populations, including how these cell types contribute to adipocyte renewal, fibrosis and inflammatory responses.
The long term goal is to develop novel approaches to promote metabolically-beneficial adipose tissue remodeling responses for reducing the risk of type 2 diabetes and related disease.
Adipose tissues are defined by the presence of specialized lipid-handling cells called adipocytes. Mammals have two main subtypes of adipocytes, white and brown. White adipocytes are specialized for energy storage and release in response to systemic demand. By contrast, brown adipocytes expend chemical energy (lipid, sugars) in the form of heat to protect animals against hypothermia during cold exposure. Brown fat-like cells, called beige adipocytes, can also be induced to develop within WAT depots in response to various stimuli, thereby augmenting thermogenic capacity.
Adipose tissues are also central players in the development and health consequences of obesity, which has reached epidemic proportions in the US and many parts of the world. Obesity is a leading cause or contributor to an expanding array of diseases such as type 2 diabetes, heart disease, stroke, arthritis, and many types of cancer. In some people, persistent weight gain overburdens the capacity of adipose tissue to safely sequester the excess nutritional energy. In these cases, the adipose tissue becomes inflamed and fibrotic, leading to ectopic deposition of lipid in liver and other tissues. This obesity-induced impairment of adipose tissue function is a primary driver of insulin resistance (pre-diabetes), fatty liver and other metabolic complications, which can eventually progress to type 2 diabetes.
Our lab is investigating mechanisms that control the development and remodeling of adipose tissue in response to external stimuli, such as cold exposure, obesity, and certain diets. In the setting of obesity, promoting adipocyte hyperplasia via the differentiation of resident progenitor cells into new fat cells is associated with improved metabolic health. Furthermore, promoting brown and beige fat cell development and function can protect against obesity and metabolic diseases.
Our projects are divided into two main areas:
(1) Brown fat biology and therapeutic potential.
Brown and beige fat can counteract obesity by expending excess nutritional energy. Increased brown adipose tissue function also promotes a healthy metabolic phenotype by burning toxic metabolites such as fatty acids, glucose, and branched chain amino acids, thereby preventing their accumulation in many organs. In humans, the amount of brown fat tissue is inversely correlated with body mass index, suggesting a potential role for brown fat in regulating body weight. Furthermore, there is great hope that brown fat-targeted therapies can be developed for obesity, fatty liver and diabetes.
Our lab is focused on identifying and understanding the mechanisms that regulate brown fat cell development and function. We are also interested in determining non-canonical functions for brown and beige fat cells in metabolic regulation.
(2) Adipose tissue remodeling responses
Adipose tissue undergoes dynamic metabolic and structural remodeling in response to various stimuli. For example, during cycles of fasting and feeding, adipocytes dramatically alter their metabolic program to accommodate the energetic needs of the organism. Upon chronic cold exposure, white adipose tissue undergoes dramatic remodeling, involving the development of thermogenic beige fat cells, recruitment of blood vessels and increased arborization of nerve fibers. During weight gain, adipose tissue can expand through metabolically beneficial adipocyte hyperplasia and/or via maladaptive adipocyte hypertrophy. In aging, adipose tissue undergoes pronounced fibrotic changes and brown fat activity is reduced.
Our lab is focused on determining the pathways that control these adipose tissue responses. We are focusing on the role of several recently identified mesenchymal cell populations, including how these cell types contribute to adipocyte renewal, fibrosis and inflammatory responses.
The long term goal is to develop novel approaches to promote metabolically-beneficial adipose tissue remodeling responses for reducing the risk of type 2 diabetes and related disease.
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论文共 129 篇作者统计合作学者相似作者
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作者统计
#Papers: 129
#Citation: 25499
H-Index: 54
G-Index: 129
Sociability: 7
Diversity: 0
Activity: 1
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