“…In the case of VMH lesions, a unique enhancement of parasympathetic vagal nerve activity is produced that is associated with increased insulin, gastric acid secretion, gastric emptying, and gastrointestinal cell proliferation (Hales and Kennedy, 1964 ; Ridley and Brooks, 1965 ; Frohman and Bernardis, 1968 ; Frohman et al, 1969 ; Han and Frohman, 1970 ; Bernardis and Frohman, 1971 ; Inoue et al, 1977 , 1983 ; Jeanrenaud, 1978 ; Berthoud and Jeanrenaud, 1979 ; Bray and York, 1979 ; Inoue and Bray, 1979 , 1980 ; Sawchenko, 1979 ; Weingarten and Powley, 1980 ; Bray et al, 1981 ; Cox and Powley, 1981a ; Bray, 1984 ; Yoshimatsu et al, 1984 ; Duggan and Booth, 1986 ; Kiba et al, 1992 , 1993 , 1996 ; Kintaka et al, 2009 ; Suzuki et al, 2014 ), which in the case of hyperinsulinemia and gastric hyperacidity is counteracted by SDV (Powley and Opsahl, 1974 ; Inoue and Bray, 1977 ; Berthoud and Jeanrenaud, 1979 ).…”