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A recent population-based genome-wide association study has revealed that the Niemann–Pick C1 ( NPC1 ) gene is associated with early-onset and morbid adult obesity. Concurrently, our candidate gene-based mouse growth study performed using the BALB/cJ NPC1 mouse model ( Npc1 ) with decreased  Npc1  gene dosage independently supported these results by suggesting an  Npc1  gene–diet interaction in relation to early-onset weight gain. To further investigate the  Npc1  gene in relation to weight gain and metabolic features associated with insulin resistance, we interbred BALB/cJ  Npc1 +/−   mice with wild-type C57BL/6J mice, the latter mouse strain commonly used to study aspects of diet-induced obesity and insulin resistance. This breeding produced a hybrid (BALB/cJ–C57BL/6J)  Npc1 +/−   mouse model with increased susceptibility to weight gain and insulin resistance. The results from our study indicated that these  Npc1 +/−   mice were susceptible to increased weight gain characterized by increased whole body and abdominal adiposity, adipocyte hypertrophy and hepatic steatosis in the absence of hyperphagia. Moreover, these  Npc1 +/−   mice developed abnormal metabolic features characterized by impaired fasting glucose, glucose intolerance, hyperinsulinemia, hyperleptinemia and dyslipidemia marked by an increased concentration of cholesterol and triacylglycerol associated with low-density lipoprotein and high-density lipoprotein. The overall results are consistent with a unique  Npc1  gene–diet interaction that promotes both weight gain and metabolic features associated with insulin resistance. Therefore, the  NPC1  gene now represents a previously unrecognized gene involved in maintaining energy and metabolic homeostasis that will contribute to our understanding concerning the current global epidemic of obesity and type 2 diabetes mellitus.

Npc1 haploinsufficiency promotes weight gain and metabolic features associated with insulin resistance