Sorry for the delayed reponse, Disski. I've been out of town for a week.
No, I didn't. The description I posted above (which is essentially what I learned in a grad. level human physiology course) regarding the digestion and absorbtion of sugars is not entirely acurate. Thanks for bringing this to my attention. Some of what I posted may very well be the case, however. I did some searching and have found that there is some controversy in the field.
The following is from a recent (2001)review. It may serve to clarify or confuse, hopefully the former. I'd be happy send a PDF copy of the original manuscript to anyone interested or you can look it up in PubMed (Bessesen, D.H., The role of carbohydrates in insulin resistance. J Nutr. 2001 Oct;131(10):2782S-2786S. Enjoy!
Simple sugars include the monosaccharides (glucose, fructose and galactose) and the dissaccharides (sucrose, maltose and lactose). Many animal studies have examined the relationship between insulin action and high intakes of fructose and sucrose (15) . Studies in rats have generally demonstrated that high intake of sucrose (18–70% of energy) or fructose (15–60% of energy) produce a decline in insulin sensitivity in the liver and later in peripheral tissues (16) . An exception to this finding is a study done in female rats that found no association between increased consumption of sucrose and insulin resistance (17) . In general, these studies have demonstrated that the adverse affects of sucrose and fructose are a function of the dose used and duration of exposure such that if a lower dose is used, the duration of exposure must be longer to produce the effect. In addition, the effects of sucrose on insulin action appear to be less in older obese rats that already have a moderate degree of insulin resistance, and in rats that are already insulin resistant as a result of consumption of a high fat diet (18) . Fructose appears to be avidly taken up and metabolized by the liver. This uptake and metabolism produce a metabolic state characterized by increased glucose uptake by the liver, which leads to a variety of cellular events, such as changes in the expression of the gluconeogenic enzymes that produce insulin resistance.
Studies in humans examining the ability of dietary sucrose to produce insulin resistance have not been nearly as convincing (3) . Studies in both normal adults and adults with type 2 diabetes have fairly consistently shown no effect on insulin sensitivity of isoenergetic substitution of sucrose or fructose for starch. Many of these studies had relatively few subjects and were of short duration. Isolated studies have shown adverse effects of dietary sucrose, but these are the exception rather than the rule. Both fructose and sucrose are associated with lower glucose excursions after ingestion, and some recommendations have even advocated the use of fructose as a beneficial sweetener for individuals with type 2 diabetes. The most recent nutritional recommendations of the American Diabetes Association do not advocate or discourage the use of these sweeteners on the basis of available data. They do caution about the development of hypertriglyceridemia with high fructose diets. Epidemiologic studies have also failed to show a relationship between fructose or sucrose consumption and the development of type 2 diabetes.
How can the discrepant results in animals and humans be reconciled? The studies done in rats suggest that if a low dose of sucrose or fructose is used, prolonged exposure is necessary to produce insulin resistance. In addition, the animal studies suggest that if adult animals or animals with preexisting insulin resistance are examined, the effects of these nutrients are reduced. Because most studies in humans have been done in older adult populations and many of the studies have been done in subjects with type 2 diabetes whose liver glucose production is already markedly elevated, it is perhaps not surprising that no effects of these nutrients has been seen.
In summary then, if sucrose has deleterious effects in humans, they are most likely to be produced in younger individuals with moderate-to-high sucrose and fructose intakes over a prolonged period. Information from human studies is not sufficient to conclusively demonstrate any adverse affects of sucrose or fructose in the diet. However, studies adequate to test this idea in younger individuals have not been done.
Complex carbohydrates are long polymers of glucose or other monosaccharides. The nomenclature attributed to these compounds can be confusing. Polymers of glucose can occur in a branched form known as amylopectin or a linear form known as amylose. Resistant starch is a term used for starches that are not directly absorbed but travel to the large intestine where they can be fermented by gut flora to produce short-chain fatty acids such as butyrate and propionate. Starch can be processed to increase the relative amount of resistant starch. Other kinds of carbohydrate polymers with nonglucose monomers such as xylose are indigestible. These complex carbohydrate molecules are the constituents of soluble or insoluble fiber. They include lignin, ß glucan, guar gum and hemicelluloses such as arabinoxylan, a major component of cereal fiber. Fiber provides minimal energy but may interact with other nutrients in the gastrointestinal tract.
In the past, complex carbohydrate consumption was thought to possibly be beneficial because of the delayed absorption of these carbohydrate polymers. However, careful studies have demonstrated that many forms of starch are absorbed as rapidly as pure glucose. The rate of absorption of complex carbohydrate depends on its chemical structure as well as methods of preparation and associated constituents of the diet. Because of its greater access to amylase, amylopectin is more rapidly digested and absorbed than amylose. Conversely, amylose appears to be more slowly absorbed and may form helices that may interact with dietary fat, slowing its absorption as well. Studies done in laboratory rats have demonstrated that high amylose diets appear to have beneficial affects on insulin sensitivity compared with high amylopectin diets (19) . Only limited data exist on amylose-rich diets in humans. What data are available suggest that there are minimal effects on insulin sensitivity, but that meals containing amylose may promote fat oxidation relative to meals containing amylopectin. Obtaining accurate information on the amylose content of various foods is very difficult, and the availability of foods that are enriched in amylose is limited.
The glycemic index (GI) has been proposed as a way in which to categorize carbohydrate foods as those that are rapidly absorbed (high GI) or more slowly absorbed (low GI) on the basis of the postingestion glucose area under the curve. Several recent studies suggested that diets that have a low GI may improve insulin sensitivity (20) and that consuming a low GI diet may be associated with a lower risk for type 2 diabetes (11 ,12) . Other studies have not shown a relationship between GI and risk for diabetes (13) . In a recent, carefully done interventional study, Kiens was unable to show any benefit to insulin sensitivity of a low GI diet as measured by the gold standard method, the euglycemic hyperinsulinemic clamp [reviewed in (3) ]. The subjects in this study were young, healthy, highly active males. The test chosen to measure insulin action examined primarily skeletal muscle insulin sensitivity. The beneficial effects of a low GI diet may be targeted primarily at the pancreas. High GI diets may tax the insulin secretory capacity of a pancreas that has acquired some limitation in this parameter. If this is true, diets with a high GI might exert their adverse effects late in the progression to type 2 diabetes. The GI has been criticized for not taking into account the interaction between the carbohydrate foodstuffs and other nutrients in the meal such as fat and protein. However, a number of recent studies have demonstrated that meals can be constructed of foods with either a high or low GI and that the postmeal glucose excursion generally follows what would be predicted from the GI of the individual foods. It is somewhat confusing, however, that the simple sugars sucrose and fructose have a very low GI and have very little stimulatory effects on insulin secretion and yet are thought to have adverse effects on insulin action. Many issues remain concerning the clinical utility of the GI, and questions remain concerning the nature of the observed effects and the underlying mechanisms.
Ingestion of foods high in dietary fiber content appears to be associated with modest beneficial effects on insulin sensitivity. Three studies have shown fiber consumption to be associated with a reduced risk of type 2 diabetes (13 ,21 ,22) . Fiber was shown to slow the postprandial rise in glucose and improve glycemic control in people with diabetes. Although there are difficulties in the nomenclature related to dietary fiber, information on the fiber content of foods is available on package labels, and there are accepted consumption guidelines. This puts fiber in a better position than amylose or GI with regard to implementing dietary change using existing food availability and labeling. In summary, it appears that the ingestion of resistant, more slowly absorbed starch may have beneficial effects on insulin sensitivity; however, data are not adequate to support widespread use of these foods to treat or prevent disease. The data relating to fiber consumption appear to be stronger, and thus it seems reasonable to advocate moderate fiber (20–30 g/d) consumption in any diet designed to improve insulin action.