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Results When compared to wildtype mice, young Alms1foz/foz mice had a significantly reduced response to insulin during ITT while no differences were observed in glucose and endogenous insulin levels during GTT. Male but not female Alms1foz/foz mice had significantly higher fasting hyperinsulinemia and HOMA-IR scores compared to wildtype littermates. Conclusions These data indicate that insulin resistance precedes obesity in young Alms1foz/foz mice at a time that beta-cell function isn’t affected. This suggests that early peripheral insulin resistance is an inherent primary consequence of the Alms1foz/foz mutation and may thereby drive the subsequent metabolic complications in this model.

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Increased insulin resistance compounded by reduced insulin sensitivity drives the "Fat Aussie" (Alms1foz/foz) model of Alström syndrome towards obesity and type 2 diabetes mellitus