Nutritional and Health Aspects of Sweeteners - Sweeteners: Nutritional Aspects, Applications, and Production Technology - page 334

Renwick and Molinary (2010) explored the interactions between sweeteners and enteroendo-
crine cells, and the consequences for glucose absorption and insulin release. A combination of in
vitro , in situ , molecular biology, and clinical studies has formed the basis of their knowledge about
the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incre-
tins by these cells. Low-energy (intense) sweeteners have been used as tools to deine the role of
intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell
lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal entero-
endocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide.
These studies have given rise to major speculations that the ingestion of food and beverages con-
taining low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the
metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimi-
lation, and appetite. However, data from numerous publications on the effects of low-energy sweet-
eners on appetite, insulin and glucose levels, food intake, and body weight have shown that there is
no consistent evidence that low-energy sweeteners increase the appetite or subsequent food intake
because of insulin release or affect blood pressure in normal subjects. Thus, the data from extensive
in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse
effects predicted by in vitro , in situ , or knockout studies in animals (Renwick and Molinary 2010).
11.2 GaStrOINteStINaL tOLeraNCe
Symptoms of carbohydrate malabsorption may include latulence, bloating, increased stool
frequency, diarrhea, or constipation. Delayed digestion and incomplete absorption may lead to
shortened intestinal transit times due to the osmotic effects of the unabsorbed polyols. Indigestible
carbohydrates reach the colon, where they feed the symbiotic colonic lora, thereby increasing the
bacterial mass and formation of bacterial fermentation products such as short chain fatty acids
(SCFAs) and gases such as hydrogen and methane. This enhanced metabolism of the intestinal lora
may inluence the colon and cause overlow diarrhea. However, gastrointestinal intolerance symp-
toms caused by polyols are transient and readily reversible when polyol consumption is stopped. The
tolerance level may increase after continuous exposure, that is, adaptation.
Polyols have a problem of limited absorption and digestibility in the small intestine, causing mal-
absorption with poorly digestible carbohydrates such as rafinose (Schiweck and Ziesenitz 1986).
The contribution of different polyols to the osmotic pressure is related to their molecular weight.
The gastrointestinal tolerance of polyols is determined by their chemical nature, the extent of diges-
tion and absorption, which are inluenced by the total quantities and portion sizes consumed, the
mode of ingestion, that is, solid or liquid, and the frequency and time of ingestion. Other dietary
components such as dietary ibers might contribute to the osmotic load and, thus, the tolerance of
the ingested polyols (Schiweck and Ziesenitz 1986).
When a slowly absorbed carbohydrate is occasionally ingested, the colonic lora is not adapted
to this substance. This could explain why different symptoms are closely correlated with the dose
of unabsorbable sugar that reaches the colon (Briet et al. 1995a,b). The tolerance of sugar alcohols
varies considerably between subjects, and it has been reported to be dose dependent (Dharmaraj et
al. 1987; Kruger et al. 1991; Livesey 1990).
Although glucose is easily absorbed and used for energy, the sorbitol moiety is only slowly
and incompletely absorbed (Lian-Loh et al. 1982; Ziesenitz and Siebert 1987). Sorbitol is slowly
absorbed by passive diffusion in the small intestine. After oral administration, it increases osmotic
pressure in the bowel by drawing in water, and is thus an osmotic laxative, sometimes leading to
diarrhea (Gatto-Smith et al. 1988). The bacterial fermentation of sorbitol in the bowel is associated
with increased latulence and abdominal cramping; 10 g of sorbitol can cause latulence and bloat-
ing, and 20 g of sorbitol can cause abdominal cramps and diarrhea.