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Gene–Diet Interactions
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Silvia Berciano, Jose M. Ordovas, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Some pioneering studies in the field of gene–diet interactions and cardiometabolic health relate to candidate genes in the path of lipoprotein metabolism, specifically associated with the APOE and the APOA1/APOC3/APOA4/APOA5 gene cluster. However, whereas there are clear and consistent associations between some of these loci and plasma lipid concentrations, the results from gene–diet interactions suffer from the similar lack of replication found for other metabolic pathways.
Association analysis of MTHFR (rs1801133 and rs1801131) and MTRR (rs1801394) gene polymorphisms towards the development of hypertension in the Bai population from Yunnan, China
Published in Clinical and Experimental Hypertension, 2023
Yongxin Liu, Chunping Xu, Yuqing Wang, Caiting Yang, Genyuan Pu, Le Zhang, Zhuang Wang, Pengyan Tao, Shenghe Hu, Mingming Lai
Patients with hypertension often have abnormal glucose or lipid metabolism. In fact, many researches focused on the influence of genetic factors on metabolic diseases, and some genetic polymorphisms have been reported to contribute to glycolipid metabolism. For example, KCNJ11, CDKAL1, and SLC2A2 gene polymorphisms could affect blood glucose level (27–29). PPM1K and UCP1 gene polymorphisms could increase TG level and decrease HDL-C level (30,31). However, APOA5 gene mutation could decrease the levels of TC, TG, and LDL-C (32). When we compared the clinical variables between hypertensive patients and the control group, significant changes were observed in FBG, TG, HDL-C, and APOA1. It was also reported that MTHFR C677T could affect the LDL-C level (33,34). Therefore, we focused on these known polymorphisms in the MTHFR gene with the biochemical variables of glycolipid metabolism. Our study showed that MTHFR C677T genetic variants could alter the levels of FBG, FMN, and APOA1 in patients with hypertension. However, Spiridonova et al. (35) found no association between MTHFR C677T and blood lipids in the western Siberian population. These contradictory results certified genetic heterogeneity across regions or ethnic groups.
Safety and efficacy of therapies for chylomicronemia
Published in Expert Review of Clinical Pharmacology, 2022
Isabel Shamsudeen, Robert A. Hegele
Potential targets for future therapies for severe HTG include apo C-II and angiopoietin-like protein 4 (ANGPTL4). Apo C-II is a co-factor for LPL, but therapies to enhance apo-CII expression would primarily be useful for the extremely small subgroup of patients (2–3%) with FCS who have apo C-II deficiency [20,86]. It is theoretically possible that stimulating or supplement apo C-II can positively affect the apo C-II to apo C-III ratio and thus promote LPL activity, but effective antagonism of apo C-III would seem to be a more efficient strategy. Finally, ANGPTL4 is a protein that regulates LPL, similar to ANGPTL3; however, preclinical trials have shown an association between ANGPTL4 inhibition and the development of mesenteric adenitis, so this target has not been pursued further [87]. Finally, APOA5 endcoding apo A-V has been considered as another drug target that when upregulated theoretcialy could reduce TG levels [56].
Treatment of hypertriglyceridemia-induced acute pancreatitis with therapeutic plasma exchange in 2 pregnant patients
Published in Journal of Obstetrics and Gynaecology, 2019
A 37-year-old primiparous woman was admitted to the gastroenterology department of our hospital with complaints of epigastric pain and nausea during her 22nd week of gestation. She had an attack history of having HTG-AP, 3 years before this attack. In the medical history, there was an uncontrolled hypertriglyceridaemia with an irregular usage of fenofibrate for 10 years. The fibrate treatment was stopped due to her pregnancy. The patient’s weight was 63 kg, and her height was 162 cm. On physical examination, her arterial blood pressure was 105/60 mmHg, heart rate was 85/min, blood temperature was 37.0 °C. A physical examination revealed a rebound tenderness on epigastrium. The laboratory results are shown in Table 1. As a result of a sequence analysis, testing for APOA5 (apolipoprotein A5) ve LIPI (LIPASE I) genetic mutation associated with hypertriglyceridaemia were negative. The results of arterial blood gas analysis were pH: 7.40, PCO2: 33.8 mmHg, PO2: 41.5 mmHg, HCO3: 22.9 mmol/L, SO2: 77.2%. The Ranson’s score was 2 at admission and at the 48th hour. We stopped the oral intake and administered an analgesic and serum saline (4–6 L/day) therapy. Haemonetics MCS+ (Haemonetics Corp. Braintree, USA) was used in TPE procedures. Fresh frozen plasma was given for TPE at a volume of 40 mL per kg of body weight (BW), as well as a heparin infusion for an anticoagulation at a rate of 10 U/kg/hour. The 3200 and 2900 mL mean plasma volumes were exchanged/substituted during the extracorporeal procedures.