Molecule Information

General Information of the Molecule (ID: Mol01892)

• Name: Lipoprotein lipase (LPL) ,Homo sapiens
• Synonyms: LPL; LIPD
• Molecule Type: Protein
• Gene Name: LPL
• Gene ID: 4023
• Location: chr8:19,901,717-19,967,259[+]
• Sequence:
  MESKALLVLTLAVWLQSLTASRGGVAAADQRRDFIDIESKFALRTPEDTAEDTCHLIPGV
  AESVATCHFNHSSKTFMVIHGWTVTGMYESWVPKLVAALYKREPDSNVIVVDWLSRAQEH
  YPVSAGYTKLVGQDVARFINWMEEEFNYPLDNVHLLGYSLGAHAAGIAGSLTNKKVNRIT
  GLDPAGPNFEYAEAPSRLSPDDADFVDVLHTFTRGSPGRSIGIQKPVGHVDIYPNGGTFQ
  PGCNIGEAIRVIAERGLGDVDQLVKCSHERSIHLFIDSLLNEENPSKAYRCSSKEAFEKG
  LCLSCRKNRCNNLGYEINKVRAKRSSKMYLKTRSQMPYKVFHYQVKIHFSGTESETHTNQ
  AFEISLYGTVAESENIPFTLPEVSTNKTYSFLIYTEVDIGELLMLKLKWKSDSYFSWSDW
  WSSPGFAIQKIRVKAGETQKKVIFCSREKVSHLQKGKAPAVFVKCHDKSLNKKSG
• Function: Key enzyme in triglyceride metabolism. Catalyzes the hydrolysis of triglycerides from circulating chylomicrons and very low density lipoproteins (VLDL), and thereby plays an important role in lipid clearance from the blood stream, lipid utilization and storage. Although it has both phospholipase and triglyceride lipase activities it is primarily a triglyceride lipase with low but detectable phospholipase activity. Mediates margination of triglyceride-rich lipoprotein particles in capillaries. Recruited to its site of action on the luminal surface of vascular endothelium by binding to GPIHBP1 and cell surface heparan sulfate proteoglycans.
• Uniprot ID: LIPL_HUMAN
• Ensembl ID: ENSG00000175445
• HGNC ID: HGNC:6677

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Insulin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Type 2 diabetes mellitus [1]

• Resistant Disease: Type 2 diabetes mellitus [ICD-11: 5A11.0]
• Resistant Drug: Insulin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Mechanism Description: Several studies have shown that lipid accumulation in liver and skeletal muscle caused by short-term HFD feeding or lipid/heparin infusions induce insulin resistance in rats. In addition, overexpression of lipoprotein lipase (LPL) in liver or muscle induced peripheral insulin resistance and the accumulation of lipid in respective tissues, and skeletal muscle-specific LPL deletion enhanced insulin signaling in HFD challenged muscle. Furthermore, deleting fat transport proteins such as CD36 or FATP-1 increased insulin-mediated glucose uptake in skeletal muscle, and liver-specific knockdown of FATP2 or FATP5 significantly reduced HFD-induced hepatosteatosis and increased glucose tolerance.

Disease- and Tissue-specific Abundances of This Molecule

ICD Disease Classification 05

Type 2 diabetes mellitus [ICD-11: 5A11]

Differential expression of molecule in resistant diseases

• The Studied Tissue: Omental adipose tissue
• The Specified Disease: Obesity related type 2 diabetes
• The Expression Level of Disease Section Compare with the Healthy Individual Tissue: p-value: 1.72E-02; Fold-change: 3.93E-01; Z-score: 9.46E-01
• The Studied Tissue: Liver
• The Specified Disease: Type 2 diabetes mellitus
• The Expression Level of Disease Section Compare with the Healthy Individual Tissue: p-value: 9.62E-01; Fold-change: -1.05E-01; Z-score: -1.85E-01

References

• Ref 1: Insulin Resistance: From Mechanisms to Therapeutic Strategies .Diabetes Metab J. 2022 Jan;46(1):15-37. doi: 10.4093/dmj.2021.0280. Epub 2021 Dec 30. 10.4093/dmj.2021.0280