In mice, O-GlcNAc's role in insulin sensitivity is further supported by the following evidence: increased resistance against diet-induced obesity upon deletion of Ogt in muscle [45], insulin resistance and dyslipidemia upon hepatic overexpression of Ogt [47], and reduced lipolysis and obesity following Ogt overexpression in the adipose tissue [48]. The gene discussed is OGT; the disease is metabolic syndrome.