What is resistant starch ?

What is resistant starch ?

Resistant starch is a form of dietary fiber that resists degradation in the small intestine by gastrointestinal enzymes with potential chemopreventive and prebiotic activity ¹. The American Association of Cereal Chemists in their annual meeting on 2001, define “Resistant starch is the portion of starch that is not digested in the human small intestine. Because humans differ in their ability to digest a particular resistant starch-containing material, there is no absolute distinction between the resistant starch and the non-resistant starch in a particular resistant starch-containing sample” ².

While most starch is digested in the upper part of the gut, resistant starch resists digestion by amylases in the small intestine and so goes all the way to the large intestine unaltered ³, ⁴. Once in the large intestine, friendly anaerobic colonic bacteria ferment the resistant starch. This process produces gasses and short chain fatty acids (SCFAs) such as acetate, butyrate, and propionate, that help to keep the lining of the bowel healthy. Butyrate has anti-inflammatory and immunoregulatory activities and butyrate appears to exert antitumor effects by inhibiting tumor cell proliferation, inducing tumor cell differentiation and apoptosis in colorectal cancer cells ⁵.

Resistant starch is starch that is not easily absorbed. Different ways of cooking can create different amounts of resistant starch. For example, resistant starch is found in slightly undercooked (‘al dente’) pasta, cooked but cooled potatoes (including potato salad), cooked and cooled grains like rice, quinoa, barley and buckwheat, under-ripe bananas, beans, lentils and a product called Hi-maize used in some breads and breakfast cereals. Freekeh, a Middle Eastern grain available in some supermarkets, is another good source. In general, foods that are less highly processed contain more resistant starch. An important benefit of resistant starch is that it ferments, which produces substances that help to keep the lining of the bowel healthy.

By far the largest proportion of the resistant starch comes from grain products for all the countries studied and as expected the source of grain products varied with the type of food consumed in large amounts, such as pasta in Italy or rice in Asia.

Fiber consumption has been proposed to contribute to weight loss through several mechanisms, including the alteration of gut motility, the attenuation of nutrient absorption, and the lowering of overall caloric intake ⁶, ⁷. In addition, fiber consumption may also enhance satiety through other mechanisms, such as adding bulk and viscosity to the intestinal content and altering the secretion of gut hormones that influence metabolism and energy expenditure ⁸, ⁹. Improved satiety and reduced food intake are common theories used to describe why fiber intake may be associated with a lower body weight ¹⁰.

Growing evidence shows that many of the chronic health conditions in developed countries could be prevented or moderated by dietary changes. The most common starchy foods in the United States diet, including white bread, cakes, and noodles, consist of a large percentage of highly digestible starch. There is concern that such rapidly digested starches may contribute to chronic disease in people and animals and, because of this problem, starches that are resistant to digestive enzymes have been the focus of a growing research emphasis. Such starches, termed resistant starches ¹¹, have been extensively reviewed in general ¹² and reviewed from the standpoint of their health properties ¹³; increasing their content in food components ¹⁴; their health and functional properties as a food ingredient ¹⁵; and their role in gut health, potentially through butyrate production ¹⁶. The estimated daily intake of resistant starch by Americans is ∼5 g per day, much less than the minimum of 6 g of resistant starch per meal recommended for health benefits ¹⁷.

Resistant Starch Classification

Englyst et al. ¹¹ proposed a classification system based on starch digestive rate. This system divides starches into rapidly digestible starches, slowly digestible starches, and resistant starches based on the results of in vitro digestion. Much of the research with resistant starch uses high-amylose products. Note that the FDA does not allow the term “resistant starch” on food labels; Hi-maize 260, a purified resistant starch product (Ingredion), is assayed for fiber content, and that amount can be placed on the food label. This product is often referred to as high-amylose maize resistant starch type 2 ¹⁸. There are currently 5 types of resistant starch (Table 1). Substantial research has been conducted on each of the 5 types of resistant starch, and they are briefly summarized next.

Resistant starch has been classified into five basic “types” ²³.

• Type 1 (resistant starch 1) is made up of starch granules surrounded by an indigestible plant matrix.
• Type 2 (resistant starch 2) occurs in its natural form such as in an uncooked potato and high amylose maize.
• Type 3 (resistant starch 3) are crystallized starches made by unique cooking and cooling processes.
• Type 4 (resistant starch 4) is a starch chemically modified by esterification, crosslinking, or transglycosylation and is not found in nature.
• Type 5 (resistant starch 5) is a starch consisting of amylose-lipid complex.

Type 1 Resistant Starch

Starch is synthesized in the endosperm of cereal grains or seeds, and starch granules are surrounded by protein matrix and cell wall material. These physical structures hinder the digestibility of starch and reduce the glycemic response ²⁴. When cooked as whole kernels or coarsely ground seeds, the thick cell wall of legume seeds and the protein matrix in cereal grains prevent water penetration into the starch in the matrix. Therefore, the starch does not have adequate moisture to readily gelatinize and swell. Without proper swelling to expose the starch molecules, the starch is not readily susceptible to enzymatic hydrolysis. The cell wall material and the protein matrix also provide a physical barrier, preventing enzymes from reaching and hydrolyzing the starch. Examples of type I resistant starch ²⁵ –containing foods are breads made with whole or coarsely ground kernels of grains ²⁶ and pasta made with durum wheat by extrusion ²⁷. Durum wheat has a high protein content and hard texture and is used for making semolina with coarse particles. Consequently, the postprandial glycemic response is substantially lower after ingesting semolina pasta compared with white bread. Residual starch that is not digested in the small intestine passes into the colon as Type 1 Resistant Starch.

Type 2 Resistant Starch

Uncooked potato starch, green banana starch, gingko starch, and high-amylose maize starch, which display the B- or C-type polymorph, are highly resistant to enzymatic hydrolysis ²⁸ and are examples of type 2 resistant starch. However, after cooking, most of the starch, such as that in baked potato and cooked banana, becomes highly digestible as a result of starch gelatinization and loss of the B- and C-type crystallites. An exception is high-amylose starch produced by mutation of the amylose-extender (ae) gene and the gene encoding starch branching-enzyme I, which has substantially longer branch chains of intermediate components and a larger proportion of amylose ²⁹, ³⁰, ³¹. Thus, this starch displays a high gelatinization temperature, above the boiling point of water. After boiling or cooking at a temperature below its gelatinization temperature, this type of starch retains its crystalline structure and remains resistant to enzymatic hydrolysis.

Type 3 Resistant Starch

Type 3 resistant starch (RSIII) is retrograded amylose and starch ³², ³³, ³⁴. Because amylose molecules have linear structures, they have a great tendency to form double helices, particularly near refrigeration temperatures (4–5°C) and with adequate moisture content. Retrograded amylose has high gelatinization temperatures, up to 170°C, and cannot be dissociated by cooking. The gelatinization temperature of retrograded amylose, however, decreases with shortening of the amylose chain length. After starchy foods are stored, particularly in a refrigerator, amylose molecules and long branch chains of amylopectin form double helices and lose their water-binding capacity. The double helices of starch molecules do not fit into the enzymatic binding site of amylase, thus they cannot be hydrolyzed by this enzyme.

Type 4 Resistant Starch

Type 4 resistant starch (RSIV) is a chemically modified starch, formed either by cross-linking ³⁵, ³⁶ or by adding chemical derivatives ³⁷. Starch with a high level of cross-linking loses the ability to swell during cooking. Consequently, the highly cross-linked starch remains in a granular form after cooking, with little enzymatic susceptibility, and cannot be hydrolyzed by amylases or fermented by microbes. Adding a chemical derivative to starch, such as octenyl succinic groups ³⁸ or acyl groups ³⁹, changes the structure of the starch and partially restricts the enzymatic hydrolysis of the starch molecule, resulting in resistant starch. A region of the starch without the derivative can be hydrolyzed by bacteria amylases and fermented to produce short-chain fatty acids.

Type 5 Resistant Starch

When starch interacts with lipids, amylose and long branch chains of amylopectin form single-helical complexes with fatty acids and fatty alcohols ³², ⁴⁰. When the linear starch chain is in a helical-complex structure with the complexed fatty acid in the cavity of the helix, starch binding and cleavage by amylase are prevented. In addition, the amylose-lipid complex also entangles amylopectin molecules, restricting the swelling of starch granules and enzyme hydrolysis ⁴¹, ⁴². Because the amylose-lipid complex formation is an instant reaction and the complex can reform after cooking, type 5 resistant starch (RSV) is considered thermally stable.

It is important to recognize that starch digestibility is influenced by nonstarch components in the digest, the structure of the starch, and starch processing before digestion. The digestibility of a given starch sample is never due to a single factor as classification systems suggest; rather, the extrinsic factor with the greatest influence on digestibility is generally used to classify the starch.

The botanical role of starch is to provide plants with a stable reserve of glucose for metabolism. The digestibility of starch is an important parameter in meeting this role. The glucose reserves must be stored in a structure that is readily available to the plant, yet able to survive for long periods of time in storage organs such as seeds or tubers. The structure of starch is complex and varies widely; however, the single structural aspect with the greatest influence on digestibility is the degree and type of crystallinity within the granule. Starch with long, linear chains has a greater tendency to form crystalline structures than starch with short, highly branched chains. Because the amylose component of starch is less branched than amylopectin, high-amylose starch tends be more resistant to digestion than low-amylose starch.

Resistant Starch Health Effects

Few studies have compared types, but one recent study by Haub et al. ⁴³ reported that cross-linked resistant starch 4 elicited a greater glucose lowering effect than the more commonly tested resistant starch 2.

In this study ⁴⁴, the researchers demonstrated that the acute ingestion of a beverage containing 26.8 g resistant starch type 2 from unripe bananas (native banana starch) reduced postprandial glucose, insulin response, and subsequent voluntary energy intake. However, there was no associated effect on subjective appetite ratings.

In another study on the effects of native banana starch (resistant starch type 2) and soy milk (control) on body weight and insulin sensitivity in obese type 2 diabetics ⁴⁵. Thirty patients who met the eligibility criteria were randomly assigned to two groups of fifteen subjects to receive either 24 g of native banana starch dissolved in 240 mL of water per day or 24 g/day of soy milk dissolved in the same volume of water for 4 weeks. After this period all data measures were collected, groups cross over to the alternate treatment group for an additional 4 weeks period after which final measures were taken at 8 weeks. There was no wash-out period between the interventions. All participants received both supplements, and on the two phases of the experiment they were instructed not to modify their diet and exercise habits. The study have shown that native banana starch (24 g per day during 4 weeks) significantly lowers body weight and increases insulin sensitivity ⁴⁵.

A majority of human studies involving resistant starch have shown a decrease in postprandial blood glucose and insulin levels. However, it is difficult to completely understand these effects due to differences in study design and the type of resistant starch used. Behall et al. ⁴⁶ found that women consuming 0.71 g, 2.57 g or 5.06 g of resistant starch had significantly lower postprandial glucose and insulin levels when compared to the control. However, this study failed to maintain an equal amount of available carbohydrate between the treatments and control. Therefore, it is difficult to determine whether the attenuation of glucose and insulin was due to the resistant starch or the fact that there was less available carbohydrate in the meal. Similarly, Reader et al. ⁴⁷ reported that 7.25 g of resistant starch added to an energy bar decreased blood glucose and insulin levels in healthy adults. But, ingredients, amount of ingredients and nutrient levels were different for each treatment. A recent study by Al-Tamimi et al. ⁴⁸ on Glucose and Insulin Responses in Humans. Al-Tamimi EK, Seib PA, Snyder BS, Haub MD. J Nutr Metab. 2010; 2010. https://www.ncbi.nlm.nih.gov/pubmed/20798767/)), however removed these variables by controlling for non starch ingredients and available carbohydrates. It was reported that postprandial blood glucose and insulin levels were significantly reduced with the supplementation of 30 g of resistant starch 4.

Several studies report that longer term consumption of a resistant starch may decrease fasting cholesterol and triglyceride levels. In a five week study, Behall et al. ⁴⁹ found that men consuming 34% of their energy from high amylose maize, when compared to a high amylopectin carbohydrate, had significantly reduced fasting cholesterol and triglyceride levels. Resier et al. ⁵⁰ reported similar results in an isocaloric and isonutrient diet with either high amylose maize or fructose. Porikos and Van Itallie ⁵¹ suggest that an interaction exists between sucrose, and therefore most likely fructose, and saturated fatty acids in turn promoting serum triglyceride levels. Interestingly, the relationship does not seem to exist for polyunsaturated fatty acids. The likely mechanism behind the ability of resistant starch to decrease cholesterol levels is an increased intestinal viscosity. However, some studies, such as Jenkins et al. ⁵², report conflicting data as  resistant starch 2 and resistant starch 3 had no effect on serum lipid profiles. While using the same type of resistant starch, subjects were only tested for two weeks. It may be that the resistant starch requires a longer period of time to promote an effect.

Research has also been conducted which evaluates the effect of resistant starch on fat oxidation and storage. However, data between studies are contradictory with no clear conclusions. Tagliabue et al. ⁵³ reported that resistant starch 2, obtained from raw potatoes, was able to increase fat oxidation 5 h postprandial. However, the test diet, consisting of the resistant starch 2, had significantly less gross and metabolizable energy. Therefore, it is difficult to determine if the increased fat oxidation was due to the resistant starch 2 or a decreased caloric intake. A 10 week study by Howe et al. ⁵⁴ may suggest the latter. High amylose starch, compared to a high amylopectin, produced no change on fat oxidation when an isocaloric diet was consumed. Conversely, Robertson et al. ⁵⁵ reported that 30 g of resistant starch 2 added to healthy subjects habitual diet resulted in a significant decrease in subcutaneous abdominal adipose tissue non-esterfied fatty acid and glycerol release. This may be a result of increased peripheral short chain fatty acid metabolism or ghrelin secretions.

Resistant Starch and Gut Bacteria

It is often recognized that the mammalian gastrointestinal (GI) tract is home to more bacterial cells than comprise the entire host. It is also well established that GI microbiota make important contributions to the health of the host, including immune system development, nutritional acquisition, and protection against infection ⁵⁶. In recent years, new evidence has greatly increased our understanding of microbiota impacts on host health. For example, an altered microbiota (dysbiosis) has been associated with human diseases, such as diabetes, obesity, inflammatory bowel diseases, and colorectal cancer ⁵⁶. GI microbiota have recently been shown to contribute to neurological diseases and influence host behavior ⁵⁷. These insights have led to a heightened interest in the role of the diet in modulation of GI microbiota as a means to improve host health ⁵⁸, ⁵⁹, ⁶⁰ and a new awareness of how diet can contribute to disease ⁵⁶, ⁶¹.

It has long been known that diet influences the microbial communities of the GI tract. Diet-induced changes in these microbiota can have beneficial effects on the health of the host through the breakdown of dietary fibers and production of SCFAs, which are an important source of energy for the host and perform important immune modulatory roles ⁶², ⁶³. Although studies to understand how different classes of resistant starch affect microbiota are limited, it is clear that high-fiber diets greatly affect the composition of mammalian microbiota ²⁵, ⁶⁴. Microbiota also reduce harmful metabolites, including bile acids, phenol, and ammonia, and influence dietary fat metabolism, which influences obesity. Changes in microbiota can occur rapidly after dietary changes. These effects can be both direct and indirect, that is, bacteria that can digest resistant starch generate energy, which provides them with a growth advantage in the gut ²⁵. Changes in community composition can also occur from decreased pH, resulting from accumulation of SCFAs ⁶⁵, ⁶⁶. Other by-products of resistant starch fermentation can be used by other classes of bacteria to enhance their abundance through metabolic cross-feeding ⁶⁷.

Although deep-sequencing studies of the impact of resistant starches on colonic microbiota have only recently been initiated, they should help identify the mechanisms by which specific bacterial taxa interact with the different forms of starch. The interindividual variation in response to dietary resistant starch will also be an important area of investigation for the therapeutic and preventive use of resistant starch to improve human health ⁶⁸.

Another topic of intense interest is the use of prebiotics to alter colonic microbiota to benefit the health of the host ⁶⁹. Although typically associated with oligosaccharides, prebiotics can represent a variety of nondigestible carbohydrates, including resistant starch ⁷⁰, that impart health benefits to the host through modulation of GI bacteria (129). Because of the interactions between GI microbiota and hosts, prebiotics, including resistant starches, have the potential to correct or prevent a variety of human diseases, including obesity, diabetes, inflammatory bowel diseases, and cancer ⁷¹, ⁷².

Resistant Starch in Prevention of Colon Cancer

Consumption of diets with abundant fiber has long been believed to protect against colorectal cancer ⁷³. More recently, resistant starch has received attention for potential prevention of colon cancer and inflammatory bowel diseases ⁶⁰. Although studies of resistant starches and human colonic health have been limited, abstracts describing 2 recent human interventions were found. In 1, a 4-wk intervention with red meat (300 g/d) increased O6-methyl-2′-deoxyguanosine adducts and genes from the microRNA-17–92 cluster (overexpressed in colorectal cancer) in the colons of humans. However, these features were not elevated with a 4-wk intervention that included red meat plus butyrylated resistant starch (40 g/d) ⁷⁴. These results suggested that resistant starch may protect the human colon against potentially damaging aspects of dietary red meat. In the second human trial, with hereditary nonpolyposis colorectal cancer gene carriers (patients with Lynch syndrome) at high risk for developing colon polyps and cancer, a diet containing 30 g/d maize starch (Novelose, Ingredion) was compared with placebo diet for 29 months. No impact on polyp or colon cancer development was observed at a 4-year follow-up ⁷⁵.

In contrast to the limited number of human interventions evaluating dietary resistant starch, several studies have been done on the impacts of resistant starch and colon cancer prevention in laboratory animals. Le Leu et al. ⁷⁶, ⁷⁷, ⁷⁸, ⁷⁹ conducted extensive studies in rats treated with the colon carcinogen azoxymethane and/or fed diets high in protein to damage the colonic epithelium. Feeding high fiber or resistant starches increased fecal bulk, fecal pH, butyrate concentration, and epithelial apoptosis, and it decreased cell proliferation markers and colon carcinogenesis. When animals were fed high levels of protein, the addition of high-amylose resistant starch reduced protein fermentation products, which paralleled reduced colorectal carcinoma development. In contrast to these findings, studies with potato fiber or potato resistant starch in rats fed control protein or high-protein diets revealed no impact of dietary resistant starches on DNA damage in the colon ⁸⁰. It is not clear whether the contrasting results are due to differences in experimental details, including the starches fed, or other factors. DNA damage was studied in rats fed diets with casein or soy protein and resistant starch (48% high-amylose maize starch), with attenuated DNA damage observed in rats fed high-protein diets and resistant starch ⁸¹. Butyrylated high-amylose corn starch was shown to be somewhat more effective than high-amylose corn starch in the inhibition of colon cancers in rats ⁸². Results from Zhao et al. ⁸³, using a novel high-amylose starch complexed with steric acid (RSV) revealed a stunning reduction in mucin-depleted foci; however, subsequent studies found that mucin-depleted foci may not be a reliable marker for subsequent colon cancer.

Numerous hypotheses have been proposed for the potential mechanism by which colon carcinogenesis may be altered by resistant starch. The most common hypotheses focus on alteration of the water-holding capacity of the fecal stream, modification of the microbiota, and increasing SCFA production. Although the SCFA hypothesis seems to have the most enthusiastic following, theories on the impacts of dietary resistant starch on the production of SCFAs and changing the microbiota are gaining momentum ⁸⁴.

SCFAs (acetate, proprionate, and butyrate) are increased in amount and concentration in many studies of resistant starch and colon health ⁶⁰, ⁷³. Butyrate, an end-product of microbial fermentation of resistant starch and the primary energy source for colonocytes, is actively transported into cells by a Na+-dependent cotransporter ⁸⁵. This cell membrane transporter serves as a tumor suppressor gene and is epigenetically silenced by hypermethylation in human aberrant crypt foci (a precancerous lesion) and colorectal cancer ⁸⁶. Butyrate has been of particular interest because of the role this molecule plays in colonic epithelial metabolism and differentiation and its influence on signaling pathways that regulate mucosal physiology ⁸⁴, ⁸⁷. In cell culture, butyrate has antitumorigenic properties, including reducing cell proliferation and inducing apoptosis of colorectal tumor cell lines ⁸⁴. However, it is not clear whether the concentrations of butyrate achieved in the colon of animals and humans fed resistant starches are optimal for the suppressive effects observed in cultured cells, because the concentrations of butyrate in animals fed control diets are higher than the concentrations of butyrate needed for suppression of colon proliferation ⁸⁸.

Colon cancer appears to develop as the result of dysregulation of molecular pathways that control epithelial proliferation, maturation, and apoptosis, with perturbations of both genetic and epigenetic components. In regeneration of normal mucosa, stem cells deep within the crypt undergo mitosis, with subsequent maturation and differentiation of daughter cells to mature absorptive and secretory populations of the colonic mucosa and eventual loss of aged or damaged cells through apoptosis. Multistep accumulation of mutations of genes in critical control pathways, coupled with changes in epigenetic factors, is believed to allow survival of abnormal crypt epithelial cells with the potential to undergo malignant transformation.

The molecular mechanisms by which dietary resistant starches are believed to alter the development or progression of colon cancer are incompletely understood. Potential mechanisms of action of dietary resistant starch on gene expression and mutation, DNA methylation, histone modification, and remodeling of chromatin are being studied intensively. Recently, animal studies identified both alterations in the microbiota and induction of protection against unrepaired DNA damage by dietary high-amylose maize starch and butyrylated high-amylose, with increased expression of genes involved in repair of DNA ⁸⁹, which, in rapidly dividing populations of the colonic mucosa, is expected to result in fewer mutations and reduced carcinogenesis. Butyrate has been also described to exert an influence on cell proliferation and differentiation through modulation of several signal transduction pathways ⁹⁰. In some colon cancer cell lines, constitutive expression of the canonical Wnt pathway, an initiating event in most colorectal cancers, is upregulated by butyrate treatment, resulting in a strong apoptotic response ⁹¹. Butyrate has also been shown to influence gene expression in the colon by modulating RNA splicing ⁹².

The potential for modification of epigenetic mechanisms, by their nature potentially reversible, by metabolic products of resistant starch also holds promise for dietary prevention of colorectal cancer. Butyrate is well known as an inhibitor of histone deacetylase, an enzyme that modifies wrapping of strands of DNA around nuclear histone proteins and thereby regulates gene transcription. Inhibitors of histone deacetylation, such as butyrate, have the ability to modify expression of genes that control cell cycle and apoptosis and function to suppress the development of pre-neoplastic and neoplastic phenotypes in vitro ⁹³. Furthermore, butyrate exerts protective effects against intestinal mucosal inflammation, a component of inflammation-mediated colorectal cancer, through apoptosis of T lymphocytes and inhibition of inducible nitric oxide synthase in colonic epithelium ⁹⁴.

The potential contributions to colonic homeostasis by endogenous or microbial products of resistant starch metabolism other than SCFAs are undetermined. Complex interactions between microbiota, dietary components, colonic epithelium, the immune system, and the nervous and endocrine systems are being dissected, and it is likely that mechanisms integrating these components will emerge.

Resistant Starch and Diabetes

Diabetes affects 8% of the United States population and 23% of the population >60 y of age, mostly as type 2 diabetes. Both type1 and type 2 diabetes are characterized by hyperglycemia, subsequently resulting in systemic tissue toxicity. Some risk factors, including increased fasting and postprandial glucose response as well as decreased insulin sensitivity and obesity, are reversible through lifestyle modifications, which were found to be more effective than pharmacological interventions in delaying the onset of type 2 diabetes ⁹⁵. One such lifestyle change is the replacement of ordinary starch in foods with resistant starch, owing to its low glycemic index. It has been reported in human studies that consuming foods, including corn porridges ⁹⁶ and crackers with a high content of resistant starch resulted in lower postprandial glucose concentrations and concomitant insulin response compared with consuming foods containing ordinary starch ⁴¹, ⁹⁷. In addition, consuming less digestible starches may decrease glycemic response to a subsequent meal, the “second meal effect.” Ten healthy individuals who ate high-amylose starch at breakfast showed decreased blood glucose response to a lunch containing highly digestible carbohydrate, compared with eating high-amylopectin starch at breakfast ⁹⁸. Consequently, replacing ordinary dietary starch with resistant starch contributes to diabetes management. Increasing consumption of resistant starch can also aid weight management, beneficially influence body composition, or both in part because food with resistant starch has lower energy concentration and has been shown in mice to reduce body fat, an important predictor of disease ⁹⁹, ¹⁰⁰. Animal models of diabetes have also demonstrated a positive effect of dietary resistant starch, such as an improvement in glycemic control in the Goto-Kakizaki rat, a nonobese model of type 2 diabetes ¹⁰¹.

The potential for low glycemic index carbohydrates, such as resistant starch, to reduce diabetic complications may be related to protection of kidney function and lead to better maintenance of adequate nutritional status, particularly with respect to vitamin D. Numerous epidemiological and case-control studies have reported vitamin D insufficiency in type 1 and type 2 diabetes ¹⁰², ¹⁰³, ¹⁰⁴. However, it is unclear whether low vitamin D exposure contributed to the onset of diabetes or whether low vitamin D status was a consequence of diabetes. The major circulating form of vitamin D, 25-hydroxycholecalciferol (25D3), circulates bound to vitamin D–binding protein (DBP) until the 25D3-DBP complex is internalized through endocytosis and activated to 1,25-dihydroxycholecalciferol by the renal proximal tubule cells or reabsorbed into the blood as 25D3 (164). In both type 1 and type 2 diabetic rats, excretion of 25D3 and DBP into the urine was markedly elevated as a result of pathologies associated with reduced expression of megalin and disabled-2, which partner together to facilitate the uptake of the 25D3-DBP complex by the kidneys ¹⁰⁵, ¹⁰⁶. However, when cornstarch in the AIN-93G rodent diet was replaced with high-amylose maize, that is, ∼37% resistant to digestion, urinary excretion of vitamin D metabolites and DBP was virtually prevented in diabetic rats ¹⁰⁵. Of interest was the finding that feeding diabetic rats the resistant starch had only a slight effect on attenuating fasting blood glucose concentrations, yet the renal expression of megalin and disabled-2 were normal, as confirmed in a type 2 diabetes rat model.

Resistant Starch and Obesity and Body Weight Management

Overconsumption of energy is proposed to be responsible for the obesity epidemic, and, as a consequence, new strategies are required to reduce energy intake (166). One potential dietary strategy is to increase consumption of dietary fiber, which has been associated with increased satiety and lower BMI ¹⁰⁷, ¹⁰⁸, ¹⁰⁹. Dietary fiber is a diverse group of carbohydrates, and large differences exist in their physical and chemical properties. Consequently, not all sources of fiber will have the same effect on satiety or body weight ¹⁰⁷. Resistant starches are proposed to provide many of the benefits of dietary fiber; therefore, they may aid weight management, although it has yet to be adequately demonstrated.

Accumulating evidence from rodent studies suggests that replacing rapidly digestible starch with resistant starch reduces body weight. Aziz et al. ¹¹⁰ found that a diet high in resistant starch reduced body weight by 40% in diet-induced obese rats. However, the diet contained 23.4% resistant starch, an amount that may not be achievable in human diets. Another study fed rats a diet containing 4%, 8%, or 16% resistant starch and found that consuming a diet with >8% resistant starch reduced adiposity compared with 0%, and for every 4% increase in resistant starch, energy intake was reduced by 9.8 kJ/d ¹¹¹. Long-term studies on the effect of increasing resistant starch consumption on body weight in humans are required.

Despite the lack of long-term studies, there are several reasons to believe that consuming resistant starch could aid weight management in humans. First, because of the lower calorie content, replacing rapidly digestible starch with resistant starch reduces the energy density of the diet ¹¹², ¹¹³. Several studies have found that reducing the energy density of the diet increases satiety and weight loss ¹¹⁴, ¹¹⁵, ¹¹⁶, ¹¹⁷.

Second, incorporating resistant starch into a meal may augment feelings of satiety. Although fiber intake has been associated with increased satiety, the effect of resistant starch on satiety is less clear. In rodent models, adding resistant starch to the diet increased secretion of the putative satiety hormones GLP-1 and PYY ¹¹², ¹¹³, suggesting that it might augment satiety. The few studies that have been conducted in humans have provided mixed results. Willis et al. (177) provided participants with low-fiber muffins or muffins supplemented with resistant starch for breakfast and found that consuming the muffins containing resistant starch promoted satiety and increased the duration of satiety. Bodinham et al. ¹¹⁸ fed males 48 g of resistant starch across 2 separate meals and found no effect on subjective appetite, although food intake was reduced by ~1300 kJ over 24 h. Conversely, a recent study that fed participants a breakfast meal containing 25 g of resistant starch had no effect on subjective appetite or food intake over the remainder of the day ¹¹⁹. This study also found that plasma concentrations of GLP-1 were lower after the resistant starch meal.

Third, resistant starch may influence body weight by increasing energy expenditure or fat oxidation. It has been proposed that replacing rapidly digestible starch with resistant starch may promote fat mobilization as the result of a reduction in insulin secretion ¹²⁰. However, currently, little evidence supports this hypothesis and several studies have failed to show that resistant starch increases energy expenditure or fat oxidation ¹²¹, ¹²², ¹²³.

Resistant Starch Foods List

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