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LITERATURE REVIEW<br />

1. Resistant starch functional and properties<br />

1.1 Definition and classification<br />

Resistant starch (RS) is described as starch that escapes digestion in the<br />

small intestine (Englyst and Kingman, 1990; Bravo et al. 1998; Topping and Clifton,<br />

2001). Scanning electron microscopy assessment of ileostomy effluents showed that<br />

some starch escaped digestion in the small intestine and the granules remained intact<br />

(Muir et al. 1995). A EURESTA study defined resistant starch as “the sum of starch<br />

and products of starch degradation not absorbed in the small intestine of healthy<br />

individuals” (Asp, 1992). Experimental data now shows that this definition could be<br />

broadened to indicate that resistant starch is not digested by pancreatic enzymes, and<br />

hence is not metabolized or absorbed in the small intestine, but rather enters the colon<br />

where it is fermented by colonic microflora. On the other hand, dietary fiber consists<br />

mainly of plant cell wall material, notably cellulose, hemicellulose, pectins, gums,<br />

mucilages and lignin. These are generally not digested by enzyme hydrolyses because<br />

of their complex nature.<br />

Classification of four forms of resistant starch and factors affecting their<br />

resistance to digestion in the colon are show in Table 1. RS is further partitioned in<br />

physically inaccessible starch (RS I), in resistant starch granules (RS II), in<br />

retrograded starch (RS III), of which only retrograded amylose is totally resistant<br />

(Englyst and Macfarlane, 1986; Englyst et al. 1987; Englyst et al. 1992; Englyst and<br />

Hudson. 1996) and in chemically modified starch (RS IV) (Brown et al. 1995).<br />

Analyses indicate that RS consists of crystallized, linear, unbranched, short-chain α-<br />

glucans (DP about 60-65) (Berry et al. 1988; Siljeström et al. 1989). Since amylose-<br />

lipid complexes significantly reduce the availability to α-amylase, an interrelation of<br />

complexation with lipids and resistant starch formation is assumed but it is verified<br />

that amylose-lipid complexes are not involved in the formation of RS.<br />

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