SHR patients treated with PEG-asparaginase (TXVI) had more severe hypertriglyceridemia (>1000 mg/dL) compared to native l-asparaginase (TXV): 10.5% versus 5.5%, respectively (P = .007).
Glycogen Storage Disease Type Ia (GSD Ia) is caused by autosomal mutations in G6PC and can present with severe hypoglycemia, lactic acidosis, and hypertriglyceridemia.
In addition, the splicing of the β-oxidation enzyme, CPT1, was altered in the SF2-RNAi flies potentially promoting the increased triglycerides in these animals.
After multivariable adjustment, ElCD was not associated with MetS (adjusted odds ratio [AOR] 1.15, 95% confidence interval [CI] 0.74, 1.78) or certain components including hypertriglyceridemia, low HDL, and high fasting glucose but was associated with central obesity (AOR 1.33, 95% CI 1.02, 1.72) and hypertension (AOR 1.50, 95% CI 1.15, 1.96), as well as higher levels of total cholesterol (3.43 vs. 3.04 mmol/L; P < 0.001), low-density lipoprotein-cholesterol (1.77 vs. 1.67 mmol/L, P = 0.002), fasting glucose (5.08 vs. 5.02 mmol/L, P = 0.022), systolic (97.57 vs. 94.69 mmHg, P < 0.001)/diastolic blood pressure (63.72 vs. 62.24 mmHg, P < 0.001), and BMI (15.46 vs. 14.83 kg/m<sup>2</sup>, P < 0.001) than SVD.
Finally, we noted a higher density of RANKL positive cells in plaques from diabetic patients as compared to non-diabetic ones and a significant positive association between hypertriglyceridemia and BMP-4 expression.
We report the first successful treatment with MCT KD in a female adult with SRSE who was refractory to classic KD with severe hypertriglyceridemia, and reviewed all SE adults with KD treatment.
Angptl4 (angiopoietin-like 4), a primary target gene of the glucocorticoid receptor in hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced by the synthetic glucocorticoid dexamethasone.
We report the first successful treatment with MCT KD in a female adult with SRSE who was refractory to classic KD with severe hypertriglyceridemia, and reviewed all SE adults with KD treatment.
We report the first successful treatment with MCT KD in a female adult with SRSE who was refractory to classic KD with severe hypertriglyceridemia, and reviewed all SE adults with KD treatment.
In addition, the subjects with central obesity, low high density lipoprotein-C (HDL-C) or hypertriglyceridemia also had significantly lower S14 levels in comparison to those without.
Interestingly, in both humans and mice, individuals with mutations in Creb3L3/CrebH, one of the Creb3 family members, exhibit hypertriglyceridemia (HTG) thus linking this transcription factor to lipid metabolism.
In addition, the splicing of the β-oxidation enzyme, CPT1, was altered in the SF2-RNAi flies potentially promoting the increased triglycerides in these animals.
In addition, AAC, AAG, GGC and AGC (rs1801260-rs11932595-rs4580704) haplotypes were analyzed: AAG was associated with higher risk of overweight (p = 0.008), hypertriglyceridemia (p = 0.040) and hypercholesterolemia (p = 0.036); GGC with lower risk of hyperglycemia (p = 0.022), better sleep pattern (p = 0.001) and with better score at mini-mental state examination (p = 0.010); AGC with lower risk of depression (p = 0.026) and AAC with lower adherence to the MD (p = 0.028).
The carriers of the SLC15A1rs1289389 T allele were found to be significantly associated with a lower risk of hypertriglyceridaemia compared with the C allele (OR = 0.54, 95% CI = 0.33-0.88, P = .013).
In addition, AAC, AAG, GGC and AGC (rs1801260-rs11932595-rs4580704) haplotypes were analyzed: AAG was associated with higher risk of overweight (p = 0.008), hypertriglyceridemia (p = 0.040) and hypercholesterolemia (p = 0.036); GGC with lower risk of hyperglycemia (p = 0.022), better sleep pattern (p = 0.001) and with better score at mini-mental state examination (p = 0.010); AGC with lower risk of depression (p = 0.026) and AAC with lower adherence to the MD (p = 0.028).