Fat caves: caveolae, lipid trafficking and lipid metabolism in adipocytes. Trends Endocrinol Metab

Department of Biochemistry Boston University School of Medicine, 72 East Concord St., Boston, MA 02118, USA.
Trends in Endocrinology and Metabolism (Impact Factor: 8.87). 05/2011; 22(8):318-24. DOI: 10.1016/j.tem.2011.04.001
Source: PubMed

ABSTRACT Caveolae are subdomains of the eukaryotic cell surface, so named because they resemble little caves, being small omega-shaped invaginations of the plasma membrane into the cytosol. They are present in many cell types, and are especially abundant in adipocytes, in which they have been implicated as playing a role in lipid metabolism. Thus, mice and humans lacking caveolae have small adipocytes and exhibit lipodystrophies along with other physiological abnormalities. In this review, we examine the evidence supporting the role of caveolae in adipocyte lipid metabolism in the context of the protein and lipid composition of these structures.

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Available from: Libin Liu, Jun 13, 2014
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    • "These cup-shaped invaginations of the plasma membrane are expressed in many cell types and are most abundant in adipocytes, endothelial and smooth muscle cells (reviewed in [3], [4], [5]). Caveolae have been suggested to play a role in a variety of pathologies, including cancer, diabetes, and cardiovascular disease and loss of caveolae causes muscular and lipodystrophies, insulin resistance and cardiovascular defects amongst a variety of other abnormalities (reviewed in [5]). Recently it has been suggested caveolae also plays a role as mechanosensor [6]. "
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    ABSTRACT: The cavins are a family of proteins associated with caveolae, cavin-1, -2 and -3 being widely expressed while cavin-4 is restricted to striated muscle. Deletion of cavin-1 results in phenotypes including metabolic changes consistent with adipocyte dysfunction, and caveolae are completely absent. Deletion of cavin-2 causes tissue-specific loss of caveolae. The consequences of cavin-3 deletion are less clear, as there are divergent data on the abundance of caveolae in cavin-3 null mice. Here we examine the consequences of cavin-3 deficiency in vivo by making cavin-3 knockout mice. We find that loss of cavin-3 has minimal or no effects on the levels of other caveolar proteins, does not appear to play a major role in formation of protein complexes important for caveolar morphogenesis, and has no significant effect on caveolae abundance. Cavin-3 null mice have the same body weight and fat mass as wild type animals at ages 8 through 30 weeks on both normal chow and high fat diets. Likewise, the two mouse strains exhibit identical glucose tolerance tests on both diets. Microarray analysis from adipose tissue shows that the changes in mRNA expression between cavin-3 null and wild type mouse are minimal. We conclude that cavin-3 is not absolutely required for making caveolae, and suggest that the mechanistic link between cavin-3 and metabolic regulation remains uncertain.
    PLoS ONE 07/2014; 9(7):e102935. DOI:10.1371/journal.pone.0102935 · 3.23 Impact Factor
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    • "Caveole is a nanosized, conelike invagination in the cytosol direction of liquiddordering of the memm brane fragment. It is determined by the polymerizaa tion of the specific protein caveolin (Pilch, Liu, 2011; Sowa, 2012). Caveolae may fuse into larger structures with a size more than 150 nm (Scherer et al., 1994). "
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    ABSTRACT: Working out of the role of lipids incorporated into membranes and the formation of a new view on the morphology, organization, and functioning of membranes has in the recent past taken place thanks to active study of the basic membrane clusters, rafts. In this overview, current data on the morphology and biophysical and biochemical features of rafts are summarized and the structure, form, and basic marker proteins of functional microdomains are described.
    Cell and Tissue Biology 11/2013; 7(6). DOI:10.1134/S1990519X13060102
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    • "Caveolae are plasma membrane microdomains enriched in cholesterol and sphingolipids. They are extremely abundant in specific cell types, including endothelial cells and adipocytes, but not in cells such as hepatocytes (Calvo et al., 2001; Pilch and Liu, 2011). Caveolin-1 (CAV1) is an integral membrane protein and, in association with PTRF/Cavin1, is the main structural protein of caveolae in nonmuscle cells. "
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    ABSTRACT: Caveolae and caveolin-1 (CAV1) have been linked to several cellular functions. However, a model explaining their roles in mammalian tissues in vivo is lacking. Unbiased expression profiling in several tissues and cell types identified lipid metabolism as the main target affected by CAV1 deficiency. CAV1-/- mice exhibited impaired hepatic peroxisome proliferator-activated receptor α (PPARα)-dependent oxidative fatty acid metabolism and ketogenesis. Similar results were recapitulated in CAV1-deficient AML12 hepatocytes, suggesting at least a partial cell-autonomous role of hepatocyte CAV1 in metabolic adaptation to fasting. Finally, our experiments suggest that the hepatic phenotypes observed in CAV1-/- mice involve impaired PPARα ligand signaling and attenuated bile acid and FXRα signaling. These results demonstrate the significance of CAV1 in (1) hepatic lipid homeostasis and (2) nuclear hormone receptor (PPARα, FXRα, and SHP) and bile acid signaling.
    Cell Reports 07/2013; 4(2). DOI:10.1016/j.celrep.2013.06.017 · 8.36 Impact Factor
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