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Peroxisome proliferator-activated receptor γ (PPARγ) gene mutations in humans and mice lead to whole-body insulin resistance and partial lipodystrophy. It is unclear whether preserved fat depots in partial lipodystrophy are beneficial for whole-body metabolic homeostasis. We analyzed the insulin response and expression of metabolic genes in the preserved fat depots of <i>Pparg^C/-</i> mice, a familial partial lipodystrophy type 3 (FPLD3) mouse model resulting from a 75% decrease in <i>Pparg</i> transcripts. Perigonadal fat of <i>Pparg^C/-</i> mice in the basal state showed dramatic decreases in adipose tissue mass and insulin sensitivity, whereas inguinal fat showed compensatory increases. Preservation of inguinal fat metabolic ability and flexibility was reflected by the normal expression of metabolic genes in the basal or fasting/refeeding states. The high nutrient load further increased insulin sensitivity in inguinal fat, but the expression of metabolic genes became dysregulated. Inguinal fat removal resulted in further impairment of whole-body insulin sensitivity in <i>Pparg^C/-</i> mice. Conversely, the compensatory increase in insulin sensitivity of the inguinal fat in <i>Pparg^C/-</i> mice diminished as activation of PPARγ by its agonists restored insulin sensitivity and metabolic ability of perigonadal fat. Together, we demonstrated that inguinal fat of <i>Pparg^C/-</i> mice plays a compensatory role in combating perigonadal fat abnormalities.