Ossabaw Island miniature swine: Cardiometabolic syndrome assessment

Abstract

Ossabaw swine were deposited on Ossabaw Island, GA, in the 1500s by Spanish explorers (Mayer and Brisbin, Jr., 1991) and, since then, the ocean has remained an impenetrable barrier to emigration of Ossabaw pigs to the mainland. Natural models of disease that arise from adaptation of animals to unique selection pressures can give insights into similar complex, multifactorial diseases in humans. Ossabaw miniature swine may recapitulate the natural pathogenesis of type 2 diabetes because of their “thrifty genotype” that enabled survival in the feast and famine ecology of Ossabaw Island. The thrifty genotype hypothesis is that in the hunter-gatherer stages of human development the ability to store excess fat enabled survival during periods of famine (Neel, 1962). In the 1970s and early 1980s, Ossabaw miniature swine were studied by ecologists for their unique adaptations in their natural habitat on Ossabaw Island (Mayer and Brisbin, Jr., 1991; Stribling et al., 1984) and, after establishment of colonies on the mainland, Ossabaws were studied by animal scientists for their propensity to obesity (Buhlinger et al., 1978; Martin et al., 1973; Martin and Herbein, 1976; Weiss et al., 1974), insulin resistance (Wangsness et al., 1977), plasma lipoproteins (Etherton and Kris-Etherton, 1980), and renal physiology (Zervanos et al., 1983). Renewed interest in Ossabaw miniature swine was sparked in 2001 with the realization of the obesity and diabetes epidemic (Bellenger et al., 2006; Mokdad et al., 2001) and Brisbin’s timely appeal to the scientific community to save feral Ossabaw Island swine from eradication by the Georgia Department of Natural Resources for environmental reasons (Brisbin and Mayer, 2001; www.state.ga.us/dnr/wild/game_mgmt/theplan.pdf, 2000). Our laboratory obtained animals from the island in an expedition in 2002 and established a breeding colony at Indiana University. We have conducted studies involving diabetes and metabolic syndrome and have made comparisons to our Yucatan model (Boullion et al., 2003; Dixon et al., 1999, 2002; Edwards et al., 2006; Hainsworth et al., 2002; Kaser et al., 2004; Lloyd et al., 2006; Mokelke et al., 2003, 2005a, 2005b; Sheehy et al., 2006; Sturek et al., 2006; Witczak et al., 2004, 2005; Zafar et al., 2004). The natural pathogenesis of type 2 diabetes involves a tendency to obesity with gradually increasing impairment of insulin action in a “prediabetes” condition, which has also been termed the metabolic syndrome or cardiometabolic risk (Eckel et al., 2005, 2006; Grundy et al., 2005; Kahn et al., 2005). In later stages, there is an increase in fasting blood glucose, which best defines diabetes. Intensive research is under way to meet the need for animal models to understand these comorbidities and develop therapies. The cardiometabolic risk or metabolic syndrome in the 9278_C018.fm Page 397 Tuesday, February 13, 2007 12:18 PM