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Quoted phrase not found in phrase index: "Hyperlipidemia due to hepatic triglyceride lipase deficiency"
Page 1
Demystifying the management of hypertriglyceridaemia.
Watts GF, Ooi EM, Chan DC. Watts GF, et al. Nat Rev Cardiol. 2013 Nov;10(11):648-61. doi: 10.1038/nrcardio.2013.140. Epub 2013 Sep 24. Nat Rev Cardiol. 2013. PMID: 24060958 Review.
Patients with hypertriglyceridaemia usually present with obesity, insulin resistance, hepatic steatosis, ectopic fat deposition, and diabetes mellitus. ...Extreme hypertriglyceridaemia requires strict dietary measures, and patients with a diagnosis of genetic lipoprotein …
Patients with hypertriglyceridaemia usually present with obesity, insulin resistance, hepatic steatosis, ectopic fat deposition, and …
Volanesorsen, an antisense oligonucleotide to apolipoprotein C-III, increases lipoprotein lipase activity and lowers triglycerides in partial lipodystrophy.
Lightbourne M, Startzell M, Bruce KD, Brite B, Muniyappa R, Skarulis M, Shamburek R, Gharib AM, Ouwerkerk R, Walter M, Eckel RH, Brown RJ. Lightbourne M, et al. J Clin Lipidol. 2022 Nov-Dec;16(6):850-862. doi: 10.1016/j.jacl.2022.06.011. Epub 2022 Sep 22. J Clin Lipidol. 2022. PMID: 36195542 Free PMC article. Clinical Trial.
BACKGROUND: Partial lipodystrophy (PL) syndromes involve deficiency of adipose tissue, causing severe insulin resistance and hypertriglyceridemia. ...CONCLUSIONS: In PL, volanesorsen decreased apoC-III and triglycerides, in part through an LPL dependent mechanism, and may …
BACKGROUND: Partial lipodystrophy (PL) syndromes involve deficiency of adipose tissue, causing severe insulin resistance and hypertri …
Lipoprotein metabolism in liver disease.
Sabesin SM, Bertram PD, Freeman MR. Sabesin SM, et al. Adv Intern Med. 1980;25:117-46. Adv Intern Med. 1980. PMID: 6987838 Review.
These abnormalities are very sensitive indicators of fundamental metabolic defects that are related in part to LCAT and apoprotein activator deficiencies, impaired H-TGL and LPL activity and, perhaps, defective remnant lipoprotein clearance by the liver. Since these abnorm …
These abnormalities are very sensitive indicators of fundamental metabolic defects that are related in part to LCAT and apoprotein activator …
USF1 deficiency activates brown adipose tissue and improves cardiometabolic health.
Laurila PP, Soronen J, Kooijman S, Forsström S, Boon MR, Surakka I, Kaiharju E, Coomans CP, Van Den Berg SA, Autio A, Sarin AP, Kettunen J, Tikkanen E, Manninen T, Metso J, Silvennoinen R, Merikanto K, Ruuth M, Perttilä J, Mäkelä A, Isomi A, Tuomainen AM, Tikka A, Ramadan UA, Seppälä I, Lehtimäki T, Eriksson J, Havulinna A, Jula A, Karhunen PJ, Salomaa V, Perola M, Ehnholm C, Lee-Rueckert M, Van Eck M, Roivainen A, Taskinen MR, Peltonen L, Mervaala E, Jalanko A, Hohtola E, Olkkonen VM, Ripatti S, Kovanen PT, Rensen PC, Suomalainen A, Jauhiainen M. Laurila PP, et al. Sci Transl Med. 2016 Jan 27;8(323):323ra13. doi: 10.1126/scitranslmed.aad0015. Sci Transl Med. 2016. PMID: 26819196
USF1 (upstream stimulatory factor 1) is a transcription factor associated with familial combined hyperlipidemia and coronary artery disease in humans. However, whether USF1 is beneficial or detrimental to cardiometabolic health has not been addressed. ...Usf1 inactivation …
USF1 (upstream stimulatory factor 1) is a transcription factor associated with familial combined hyperlipidemia and coronary artery d …
Environmental modulation of atherosclerosis end points in familial hypercholesterolemia.
Hegele RA. Hegele RA. Atheroscler Suppl. 2002 Mar;2(3):5-7. doi: 10.1016/s1567-5688(01)00013-7. Atheroscler Suppl. 2002. PMID: 11923122 Review.
Anecdotal examples of apparent modulation of atherosclerosis severity by lifestyle changes were also seen in other monogenic metabolic problems, such as hepatic lipase deficiency and Dunnigan-type familial partial lipodystrophy. ...
Anecdotal examples of apparent modulation of atherosclerosis severity by lifestyle changes were also seen in other monogenic metabolic probl …
Lysosomal acid lipase deficiency in all siblings of the same parents.
Maciejko JJ, Anne P, Raza S, Lyons HJ. Maciejko JJ, et al. J Clin Lipidol. 2017 Mar-Apr;11(2):567-574. doi: 10.1016/j.jacl.2017.02.006. Epub 2017 Feb 22. J Clin Lipidol. 2017. PMID: 28502515
We present 4 normal-weight sibling children with lysosomal acid lipase deficiency (LAL-D). LAL-D was considered in the differential diagnosis based on the absence of secondary causes and primary inherited traits for their marked hyperlipidemia, together with …
We present 4 normal-weight sibling children with lysosomal acid lipase deficiency (LAL-D). LAL-D was considered in the differe …
Effect of a common missense variant in LIPA gene on fatty liver disease and lipid phenotype: New perspectives from a single-center observational study.
Pasta A, Borro P, Cremonini AL, Formisano E, Tozzi G, Cecchi S, Fresa R, Labanca S, Djahandideh A, Sukkar SG, Picciotto A, Pisciotta L. Pasta A, et al. Pharmacol Res Perspect. 2021 Oct;9(5):e00820. doi: 10.1002/prp2.820. Pharmacol Res Perspect. 2021. PMID: 34476902 Free PMC article.
Lysosomal acid lipase deficiency (LAL-D) is an autosomal recessive disease characterized by hypoalphalipoproteinemia, mixed hyperlipemia, and fatty liver (FL) due to mutations in LIPAse A, lysosomal acid type (LIPA) gene. ...The presence of rare allele caused …
Lysosomal acid lipase deficiency (LAL-D) is an autosomal recessive disease characterized by hypoalphalipoproteinemia, mixed hy …
Familial lipoprotein lipase-activity deficiency: study of total body fatness and subcutaneous fat tissue distribution.
Brun LD, Gagné C, Julien P, Tremblay A, Moorjani S, Bouchard C, Lupien PJ. Brun LD, et al. Metabolism. 1989 Oct;38(10):1005-9. doi: 10.1016/0026-0495(89)90013-9. Metabolism. 1989. PMID: 2796749
Eleven were males, aged 10 to 57 years, and eight were females, aged 13 to 46 years. Familial lipoprotein-lipase-activity deficiency was diagnosed by the absence of lipoprotein-lipase activity in the plasma withdrawn ten and 20 minutes after intravenous injec …
Eleven were males, aged 10 to 57 years, and eight were females, aged 13 to 46 years. Familial lipoprotein-lipase-activity deficien …
Detection of missense mutations in the genes for lipoprotein lipase and hepatic triglyceride lipase in patients with dyslipidemia undergoing coronary angiography.
Moennig G, Wiebusch H, Enbergs A, Dorszewski A, Kerber S, Schulte H, Vielhauer C, Haverkamp W, Assmann G, Breithardt G, Funke H. Moennig G, et al. Atherosclerosis. 2000 Apr;149(2):395-401. doi: 10.1016/s0021-9150(99)00330-5. Atherosclerosis. 2000. PMID: 10729390 Clinical Trial.
Coronary events have a close association with a low HDL/hypertriglyceridemia (LHDL/HTG) phenotype. As enzymes that hydrolyze triglyceride-rich lipoproteins are associated with a modulation of both HDL cholesterol and triglycerides, we have tested the hypothesis that mutati …
Coronary events have a close association with a low HDL/hypertriglyceridemia (LHDL/HTG) phenotype. As enzymes that hydrolyze triglyceride …
Transient lipoprotein lipase deficiency with hyperchylomicronemia.
Goldberg IJ, Paterniti JR Jr, Franklin BH, Ginsberg HN, Ginsberg-Fellner F, Brown WV. Goldberg IJ, et al. Am J Med Sci. 1983 Sep-Oct;286(2):28-31. doi: 10.1097/00000441-198309000-00005. Am J Med Sci. 1983. PMID: 6614044
The postheparin plasma hepatic triglyceride lipase was normal. Tests for associated systemic diseases were negative. Six weeks after presentation, that patient's lipoprotein levels and postheparin plasma lipase activities were normal. This was a unique …
The postheparin plasma hepatic triglyceride lipase was normal. Tests for associated systemic diseases were negative. Si …
18 results