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The objective of the study was to examine the potential differential effect of insulin and acipimox (both of which reduce free fatty acid [FFA] availability) on VLDL apolipoprotein (apo) B metabolism. We studied eight healthy men (age 40 +/- 4 years, BMI 25.8 +/- 0.9 kg/m2, plasma triglycerides 1.30 +/- 0.12 mmol/l) after an overnight fast (control study, n = 8), during inhibition of lipolysis with an antilipolytic agent, acipimox (n = 8), and under 8.5-h euglycemic-hyperinsulinemic conditions (n = 5). Plasma FFAs were similarly suppressed in the acipimox and insulin studies (approximately 70% suppression). 2H3-leucine was used to trace apo B kinetics in VLDL1 and VLDL2 subclasses (Svedberg flotation rates: 60-400 and 20-60), and a non-steady-state multicompartmental model was used to derive the kinetic constants. The mean rate of VLDL1 apo B production was 708 +/- 106 mg/day at the beginning and 602 +/- 140 mg/day at the end of the control study. Production of the lipoprotein decreased to 248 +/- 93 mg/day during the insulin study (P < 0.05 vs. control study) and to 375 +/- 92 mg/day (NS) during the acipimox study. Mean VLDL2 apo B production was significantly increased during the acipimox study (399 +/- 42 vs. 236 +/- 27 mg/day, acipimox vs. control, P < 0.05) but not during the insulin study (332 +/- 51 mg/day, NS). The fractional catabolic rates of VLDL1 and VLDL2 apo B were similar in all three studies. We conclude that acute lowering of FFAs does not change the overall production rate of VLDL particles, but there is a shift toward production of smaller and denser VLDL2 particles, and, thus, the amount of total VLDL particles secreted remained constant. Insulin acutely suppresses the total production rate of VLDL apo B by decreasing the production of large triglyceride-rich VLDL1 particles. Based on these findings, we postulate that insulin has a direct suppressive effect on the production of VLDL apo B in the liver, independent of the availability of FFAs.

During mating in the Lepidoptera (moths and butterflies), sperm are passed to the female via a copulation in which the male transfers a large and often complex spermatophore over the major part of an hour or more. Subsequently, over the course of an hour or often considerably more, the sperm exit the spermatophore and travel over a relatively complex route to the spermatheca, where the sperm are stored and then used as the eggs are laid. The process of spermatophore formation and migration of sperm in the female has been described in many Lepidoptera, but the mechanics involved have received less attention. Understanding these is important in discerning the relative roles of males and females in determining the outcome of matings. We describe how the spermatophore is formed, how the sperm migrate in the female, and the fate of the sperm in the spermatheca of the tobacco hornworm moth, Manduca sexta. We found that sperm movement from the spermatophore relied upon motility of the sperm, but further movement of the sperm to the spermatheca was dependent on female muscular action. After arriving in the spermatheca, the anucleate parasperm (apyrene sperm) separated into the lateral pouch of the spermatheca (lagena) and disappeared over 7 days, whereas the eusperm (eupyrene sperm) persisted in the central lumen of the spermatheca (utriculus). The relative persistence of these two sperm types could shed some light on what determines the proclivity of females to remate. Elucidation of these physiological mechanisms contributes to an understanding of the mechanisms of female choice and male competition in Lepidoptera.

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