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Adrenergic-receptor beta2 ( ADRB2 ) and beta3 ( ADRB3 ) are obesity genes that play a key role in the regulation of energy balance by increasing lipolysis and thermogenesis. The  Glu27  allele in  ADRB2  and the  Arg64  allele in  ADRB3  are associated with abdominal obesity and early onset of non-insulin-dependent diabetes mellitus (NIDDM) in many ethnic groups. Peroxisome proliferator-activated receptor γ ( PPARG ) is required for adipocyte differentiation.  Pro12Ala  mutation decreases PPARG activity and resistance to NIDDM. In humans, energy-expense alleles,  Gln27  in  ADRB2  and  Trp64  in  ADRB3 , are at higher frequencies than  Glu27  and  Arg64 , respectively, but  Ala12  in  PPARG  is at lower frequency than  Pro12 . Adaptation of humans for lipolysis, thermogenesis, and reduction of fat accumulation could be considered by examining which alleles in these genes are dominant in non-human primates (NHP). All NHP ( P. troglodytes ,  G. gorilla ,  P. pygmaeus ,  H. agilis  and macaques) had energy-thrifty alleles,  Gly16  and  Glu27  in  ADRB2 , and  Arg64  in  ADRB3 , but did not have energy-expense alleles,  Arg16 ,  Gln27  and  Trp64  alleles. In  PPARG  gene, all NHP had large adipocyte accumulating type, the  Pro12  allele.   Conclusions  These results indicate that a tendency to produce much more heat through the energy-expense alleles developed only in humans, who left tropical rainforests for savanna and developed new features in their heat-regulation systems, such as reduction of body hair and increased evaporation of water, and might have helped the protection of entrails from cold at night, especially in glacial periods.

Human-Specific SNP in Obesity Genes, Adrenergic Receptor Beta2 (ADRB2), Beta3 (ADRB3), and PPAR γ2 (PPARG), during Primate Evolution