Sex steroids mediate discrete effects on HDL cholesterol efflux capacity and particle concentration in healthy men

Abstract

Testosterone deprivation in healthy men leads to a dissociation between changes in serum HDL-C and HDL CEC. Changes in serum HDL-C specifically due to testosterone exposure may not reflect changes in HDL function.

High Density Lipoprotein Cholesterol Efflux Capacity and Atherosclerosis in Cardiovascular Disease: Pathophysiological Aspects and Pharmacological Perspectives

“…The decrement in HDL function may thus suggest that a reduction in the amounts and/or efficiency of either small or large HDL [ 32 , 162 ], or HDL remodeling [ 163 ] may occur in hypogonadism. In middle-aged subjects, medically castrated by the gonadotropin-releasing hormone antagonist acyline, HDL-C rises were reported, but not effect was observed on HDL CEC [ 164 ]. The same pharmacological castration procedure in young healthy men increased both HDL-C and HDL CEC [ 165 ].…”

The effect of transgender hormonal treatment on high density lipoprotein cholesterol efflux capacity

“…Studies on the association between testosterone and HDL-CEC have not provided conclusive information, e.g., no differences were observed in HDL-CEC before and after treatment in chemically castrated healthy adult males or older hypogonadal men 43,44 . This finding is similar to the absence of changes in HDL-CEC in trans men in the present study.…”

<p>Hypertriglyceridemia-Related Pancreatitis In Patients With Type 2 Diabetes: Links And Risks</p>

“…The prevalence of HTG in western societies approaches 25% to 30% and is correlated with features of the metabolic syndrome 12. The rate of severe HTG is significantly lower, reported as 1.7% when a cutoff of >500 mg/dL is used,13 and 0.1–0.4% with HTG >1000 mg/dL in different populations 14–17. Varying triglyceride cutoffs were suggested over the years by professional groups for defining “severe HTG”.…”

“…Elevated triglyceride levels in serum are associated with increased risk for acute pancreatitis, which is particularly observed in severe HTG. Triglyceride levels above 500 mg/dL or 1000 mg/dL are common thresholds for initiating lipid-modifying agents for reducing the risk of developing pancreatitis, though it is thought that values triggering acute pancreatitis often exceed 2000–3000 mg/dL 29,30. The risk may depend on the type and characteristics of the circulating triglyceride-rich lipoproteins, with the greater risk associated with higher circulating levels of chylomicrons.…”

“…The rate of acute pancreatitis in patients with severe HTG may reach 15–20%,31 and in a recent study from an integrated health-care system it was shown that for each 100 mg/dL unit of increase in the triglyceride levels above 1000 mg/dL, there was a 3% increase in risk of developing pancreatitis 32. Nevertheless, although a gradual stepwise increase in the risk of acute pancreatitis is clearly observed in patients with severe (1000–2000 mg/dL), very-severe (2000–3000 mg/dL) and extreme (>3000 mg/dL) hypertriglyceridemia,17 a large retrospective epidemiological study has shown that even mild-to-moderate HTG, from values of 177 mg/dL and above, was associated with a consecutive increase in the risk of acute pancreatitis 33. It is possible that the risk of developing pancreatitis is not uniform in its relation with HTG, and that HTG might be both a cause and an effect of other metabolic factors associated with pancreatitis including diabetes, obesity and alcohol use, that when uncontrolled, acute pancreatitis may be triggered.…”