As an absence of hepatic leptin signaling leads to elevated triglyceride levels in VLDL particles,28 the production of triglyceride-rich VLDL is likely associated with leptin deficiency in ob/ob mice.29 The maintenance of LPL activity in LCKD-fed ob/ob mice could also accelerate the release of triglycerides to extrahepatic tissues. Here, LPL is linked to hyperinsulinemic hypoglycemia, familial, 4.