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Journal of Lipid Research
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    • Abumrad, Nada A1
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    • Commentaries
      Open Access

      Intramuscular adipocytes: a buried adipose tissue depot deserving more exploration

      Journal of Lipid Research
      Vol. 60Issue 4p753–754Published online: January 4, 2019
      • Lori Begaye
      • Judith A. Simcox
      Cited in Scopus: 3
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        Adipocytes in the skeletal muscle are cellular populations that directly communicate nutrient stores to muscle and regulate glucose homeostasis (1). There are multiple depots of adipocytes in skeletal muscle, including intermuscular adipocytes found in the space between muscle groups, and intramuscular adipocytes, which are located between muscle fibers. The intramuscular adipocyte population is becoming an area of research focus because it is an important measure of meat quality for the livestock industry and is associated with adverse human health conditions, including obesity and sarcopenia (2).
      • Commentaries
        Open Access

        Regulation of lipophagy in NAFLD by cellular metabolism and CD36

        Journal of Lipid Research
        Vol. 60Issue 4p755–757Published online: January 28, 2019
        • Dmitri Samovski
        • Nada A. Abumrad
        Cited in Scopus: 10
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          Nonalcoholic fatty liver disease (NAFLD) progresses in a subset of patients to nonalcoholic steatohepatitis (NASH) with inflammation, fibrosis, and increased risk of hepatocellular carcinoma (1). A better understanding of the factors involved in the development, progression, or resolution of hepatic steatosis and NAFLD will expand the repertoire of tools available for treatment of NASH and its associated comorbidities.
          Regulation of lipophagy in NAFLD by cellular metabolism and CD361
        • Commentary
          Open Access

          The ceramide ratio: a predictor of cardiometabolic risk

          Journal of Lipid Research
          Vol. 59Issue 9p1549–1550Published online: July 9, 2018
          • Trevor S. Tippetts
          • William L. Holland
          • Scott A. Summers
          Cited in Scopus: 28
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            Circulating lipids drive the tissue dysfunction that underlies cardiovascular disease and diabetes. Clinical indices of risk of these metabolic disorders include serum levels of LDLs, total and LDL-cholesterol, and triglycerides, all of which reveal heightened susceptibility for major adverse cardiac events (MACEs). Despite their widespread use, these established clinical biomarkers only weakly forecast cardiovascular outcomes, leaving substantial need to develop more reliably predictive diagnostic tests.
          • Commentary
            Open Access

            Hepatic thyroid hormone receptor β1 agonism: good for lipids, good for bile?

            Journal of Lipid Research
            Vol. 59Issue 9p1551–1553Published online: July 31, 2018
            • Paul A. Dawson
            • Paolo Parini
            Cited in Scopus: 2
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              Hepatic bile formation plays an essential role in lipid digestion and absorption, cholesterol homeostasis, and excretion of lipid soluble metabolites and xenobiotics. Bile is a complex, lipid-rich micellar solution composed primarily of water, inorganic solutes, and organic solutes such as amphipathic conjugated bile acids (BAs), the membrane phospholipid phosphatidylcholine (PC), cholesterol, bile pigments, and endogenous metabolites (1). The major organic solutes, BAs, phospholipids, and cholesterol are termed “biliary lipids” and their secretion into bile is mediated by three distinct canalicular membrane ABC transporters, ABCB11(BSEP), ABCB4 (MDR3) (Abcb4/Mdr2 in rodents), and ABCG5/ABCG8, respectively (1).
              Hepatic thyroid hormone receptor β1 agonism: good for lipids, good for bile?1
            • Commentary
              Open Access

              AIBP, inflammation, and atherosclerosis

              Journal of Lipid Research
              Vol. 59Issue 7p1081–1083Published online: May 4, 2018
              • Hainan Chen
              • Kai Yin
              Cited in Scopus: 6
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                Atherosclerosis (AS), a major etiology of cardiovascular disease, is considered to be a chronic inflammatory disease characterized by excessive inflammatory cells, such as macrophages, accumulated in the arterial wall (1). As the main effector cells of the immune/inflammatory system, macrophages engulf lipids and produce various inflammatory factors, thus participating in the progress of AS (1–3). Therefore, it is very important to clarify the mechanisms that regulate macrophage-related inflammatory response for the prevention of AS.
                AIBP, inflammation, and atherosclerosis1
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