Adipose tissue remodeling in pathophysiology of obesity

Lee, Mi‐Jeong; Wu, Yuanyuan; Fried, Susan K.

doi:10.1097/mco.0b013e32833aabef

Cited by 169 publications

(125 citation statements)

References 61 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…However, adipose tissue is highly dynamic with a constant turnover of adipocytes and de novo differentiation of adipocytes from precursor populations (Lee et al, 2010a). Thus, to explore therapeutic avenues to target individual adipose depots or even adipocyte populations, the source of adipocytes in adult tissues needs to be understood and considered.…”

Section: Origins Of Adult Adipose Tissue Progenitor Cellsmentioning

confidence: 99%

Heterogeneity of adipose tissue in development and metabolic function

Schoettl

Fischer

Ussar

2018

Journal of Experimental Biology

163

133

View full text Add to dashboard Cite

Adipose tissue is a central metabolic organ. Unlike other organs, adipose tissue is compartmentalized into individual depots and distributed throughout the body. These different adipose depots show major functional differences and risk associations for developing metabolic syndrome. Recent advances in lineage tracing demonstrate that individual adipose depots are composed of adipocytes that are derived from distinct precursor populations, giving rise to different populations of energy-storing white adipocytes. Moreover, distinct lineages of energy-dissipating brown and beige adipocytes exist in discrete depots or within white adipose tissue depots. In this Review, we discuss developmental and functional heterogeneity, as well as sexual dimorphism, between and within individual adipose tissue depots. We highlight current data relating to the differences between subcutaneous and visceral white adipose tissue in the development of metabolic dysfunction, with special emphasis on adipose tissue expansion and remodeling of the extracellular matrix. Moreover, we provide a detailed overview of adipose tissue development as well as the consensus and controversies relating to adult adipocyte precursor populations.

show abstract

Section: Origins Of Adult Adipose Tissue Progenitor Cellsmentioning

confidence: 99%

Heterogeneity of adipose tissue in development and metabolic function

Schoettl

Fischer

Ussar

2018

Journal of Experimental Biology

163

133

View full text Add to dashboard Cite

show abstract

“…Excessive accumulation of adipose tissue in obesity is frequently associated with metabolic defects (postprandial hyperglycaemia, dyslipidaemia, insulin resistance) that may lead to type 2 diabetes and cardiovascular diseases (hypertension, atherosclerosis, nephropathies) [1,2]. In parallel with its lipid storage capacity, the adipose tissue produces various bioactive molecules (adipokines, reactive phospholipids, glycerol, NEFA).…”

Section: Introductionmentioning

confidence: 99%

Lysophosphatidic acid impairs glucose homeostasis and inhibits insulin secretion in high-fat diet obese mice

et al. 2013

View full text Add to dashboard Cite

Aims/hypothesis Lysophosphatidic acid (LPA) is a lipid mediator produced by adipocytes that acts via specific Gprotein-coupled receptors; its synthesis is modulated in obesity. We previously reported that reducing adipocyte LPA production in high-fat diet (HFD)-fed obese mice is associated with improved glucose tolerance, suggesting a negative impact of LPA on glucose homeostasis. Here, our aim was to test this hypothesis. Methods First, glucose tolerance and plasma insulin were assessed after acute (30 min) injection of LPA (50 mg/kg) or of the LPA1/LPA3 receptor antagonist Ki16425 (5 mgkg −1 day −1 , i.p.) in non-obese mice fed a normal diet (ND) and in obese/prediabetic (defined as glucose-intolerant) HFD mice. Glucose and insulin tolerance, pancreas morphology, glycogen storage, glucose oxidation and glucose transport were then studied after chronic treatment (3 weeks) of HFD mice with Ki16425. Results In ND and HFD mice, LPA acutely impaired glucose tolerance by inhibiting glucose-induced insulin secretion. These effects were blocked by pre-injection of Ki16425 (5 mg/kg, i.p.). Inhibition of glucoseinduced insulin secretion by LPA also occurred in isolated mouse islets. Plasma LPA was higher in HFD mice than in ND mice and Ki16425 transiently improved glucose tolerance. The beneficial effect of Ki16425 became permanent after chronic treatment and was associated with increased pancreatic islet mass and higher fasting insulinaemia. Chronic treatment with Ki16425 also improved insulin tolerance and increased liver glycogen storage and basal glucose use in skeletal muscle. Conclusions/interpretation Exogenous and endogenous LPA exerts a deleterious effect on glucose disposal through a reduction of plasma insulin; pharmacological blockade of LPA receptors improves glucose homeostasis in obese/prediabetic mice.

show abstract

“…In response to increases in fat mass, as seen in obesity, the adipose tissue undergoes distinct structural remodeling (1). Recent attention has focused on the importance of the extracellular matrix (ECM) in remodeling of adipose tissue during the development of obesity.…”

mentioning

confidence: 99%