The World Health Organization defines overweight and obesity as abnormal or excessive fat accumulation that may impair health. In dogs, overweight is considered the point at which body weight is > 15% over ideal body weight, whereas obesity is defined as the point at which body weight exceeds 30% over ideal body weight.1 There has been a dramatic increase in obesity in the United States during the past 2 decades. In 1 study,2 investigators conducted a survey in 1999 and 2000 to determine the prevalence of obesity for a diverse population of 4,115 adult men and women regarded as a nationally representative sample of the US population. They reported that 64.5%, 30.5%, and 4.7% of this population were considered overweight, obese, and extremely obese, respectively, as determined on the basis of body mass index. A similar survey2 was conducted in 1988 through 1994, for which the prevalence of overweight, obese, and extremely obese humans was 55.9%, 22.9%, and 2.9%, respectively. A survey3 conducted during 2003 and 2004 revealed that 32.2% of US adults were obese. In concert with these estimates, it appears that the condition of obesity in humans is also reflected in obesity in dogs. For example, 22.4% to 40.0% of adult dogs in Western countries are considered overweight and obese.4,5 In the United States in 1995, the prevalence of adult dogs considered overweight and obese was 34.1%.6 In Australia in 2005, 33.5% of dogs were considered overweight and 7.5% were obese.4 In a studya conducted in 2006, it was found that 29.2% of pet dogs in Japan were obese. Thus, similar to the condition in humans, obesity in dogs is also a problem throughout the world.
One approach for weight management is to alter lipid metabolism by enhancing fat mobilization and utilization to prevent lipid absorption or enhance satiety. The extent to which dietary supplements or diet components can help achieve these goals has been the subject of considerable debate.7,8 Some supplements for this purpose include various fiber types, DAG, and LGI starch. All have been evaluated for their effects on weight loss.8–13 However, which of these nutrients (if any) can successfully achieve efficient and healthy weight loss by modifying lipid metabolism in dogs or humans has not been clearly established. Therefore, the intent of this review is to summarize the potential for weight management by use of these nutrients.
Dietary Fiber
Dietary fiber generally refers to plant components, including plant cell wall substances (cellulose, hemicelluloses, pectin, and lignin) and intracellular polysaccharides (gums and mucilage) that are resistant to hydrolysis by digestive enzymes.14 Dietary fiber is classified into insoluble and soluble fiber on the basis of water solubility. Insoluble fiber, such as cellulose, hemicellulose, and lignin, resists fermentation by microorganisms in the intestines; thus, it is also called nonfermentable fiber. In contrast, most of the soluble fibers, including inulin, pectins, gums, and fructooligosaccharides, are fermented by intestinal microorganisms and yield short-chain fatty acids; thus, they are also called fermentable fibers.15
Dietary fibers have many functions and activities as they transit through the gastrointestinal tract. For example, diets that contain dietary fiber generally have a lower energy density and require more mastication, which leads to secretion of more saliva and gastric acid and, with increased stomach distention, may result in increased satiety.16 Moreover, soluble fiber induces a viscous solution in the gastrointestinal tract by absorbing water. This viscous fiber is considered to slow digestion of foods by capturing nutrients, including fats, digestive enzymes, and bile acids.17 This phenomenon also delays nutrient absorption. A slow rate of gastric emptying also potentially provides satiety.18,19 Therefore, long-term intake of dietary fiber potentially reduces body weight by decreasing daily food intake as a result of an increase in satiety. In addition, the delay in digestion and absorption caused by dietary fiber may result in a decrease in concentrations of plasma lipids (such as TAG and cholesterol). Furthermore, dietary fiber can bind bile acids. These bile acids can then be excreted in the feces, which, in some cases, can result in a sufficiently large enough loss that it increases bile acid synthesis from cholesterol in the liver.20,21 Although the mechanism is not fully understood, viscous dietary fiber can decrease plasma cholesterol concentrations in a dose-dependent manner.22
Studies in humans and rats—It appears that there is a conclusive satiety effect of dietary fiber in humans.23–26 For example, investigators in 1 study23 reported a decrease in energy intake in previously obese adult women by use of fiber supplementation. In that study, the subjects were provided 20 g of guar gum in orange juice twice a day during the afternoon and evening for 1 week. Average daily energy intake by use of fiber supplementation was significantly lower than that for no fiber supplementation, and fiber supplementation did not decrease satiety or increase hunger, which were measured by use of a 100-mm visual analogue scale. Moreover, when energy intake was restricted by 955.6 kcal/d, subjects given the fiber supplement were significantly less hungry than subjects given no supplement.23
In another study,25 investigators also evaluated the satiety effect of dietary fiber. They provided a fiber mixture (3 g of Plantago ovata husk and 1 g of glucomannan) or a placebo 2 or 3 times/d for 16 weeks. Results included an increase in satiety (determined by use of a 100-mm visual analogue scale) for the groups receiving the fiber mixture. Also, weight loss typically was greater for the fiber mixture groups than for the placebo group; however, weight loss did not differ significantly among groups. The effect of dietary fiber on weight loss is somewhat inconsistent, whereas the effect of dietary fiber on satiety has been conclusively verified.27–31
Regarding the effects of dietary fiber on lipid metabolism, investigators in 1 study25 detected a decrease in plasma total cholesterol and LDL-cholesterol concentrations when subjects were provided fiber supplementation for 16 weeks, compared with results for the placebo group. However, TAG concentration in that study did not differ significantly among the groups. In contrast, investigators in another study32 evaluated feeding a mixture of 2 soluble fiber types to clinically normal and diabetic rats for 2 to 4 weeks. They determined that soluble fiber significantly lowered plasma cholesterol and TAG concentrations and food intake. Other investigators26 also reported cholesterol- and TAG-lowering effects when hypercholesterolemic men were given 21.5 g of dietary fiber/1,000 kJ for 24 weeks, although the fiber type was not specified in that study. Therefore, dietary fiber (ie, soluble fiber) appears to decrease plasma lipid concentrations.
The proposed mechanisms by which soluble fiber decreases plasma lipid concentrations have been elucidated in studies33–36 involving rats. For example, when rats were given wheat bran and wheat germ (10% of the weight of a meal) through a gastric catheter for 4 weeks, gastric and intestinal TAG lipolysis was significantly decreased.36 Moreover, rats given wheat bran and wheat germ in that study decreased their mucosal uptake of radiolabled lipid fractions originating from [14C] triolein and [3H] cholesterol (which were added to the test meal) while increasing the accumulation of these lipids and cholesterol in the cecum. As a consequence, plasma [14C] lipid fractions and [3H] cholesterol concentrations were significantly decreased by both wheat bran and wheat germ. Together these results indicate that soluble fiber decreases plasma lipid concentrations as a result of less digestion and absorption of lipids in the gastrointestinal tract.
Studies in dogs—Food intake, weight loss, and hypolipidemic effects of dietary fiber have been intensively studied in humans and rodents; however, its effects in dogs have been somewhat inconclusive. For example, 1 study37 was performed in which adult female English Pointers were fed 0% to 12.5% of the diet (dry-matter basis) in the form of beet pulp for 2 weeks. Incremental addition of beet pulp in the diets did not alter energy intake, whereas dry-matter intake was slightly higher when increased amounts of beet pulp were added to the diets. Moreover, other investigators19,38 also have reported that 12.9 to 99.1 g of dietary fiber/1,000 kcal affected neither calorie nor dry-matter intake (number of grams) in adult dogs. However, it should be mentioned that the food offered in those studies19,38 was highly restricted (energy offered, approx 50 kcal/body weight0.75/d × body weight0.75) in an attempt to induce weight reduction. Therefore, results for energy and dry-matter intake may more likely have been affected by food restriction than by fiber supplementation. By contrast, investigators in another study39 detected a reduction of calorie intake by the inclusion of dietary fiber (29% of diet) in a diet formulated for dogs. In support of this finding, 2 other studies40,41 revealed that when diets containing 12% to 21% crude fiber (on an as-fed basis) were fed, dogs fed the diet with fiber consumed less metabolizable energy than did dogs fed a diet containing only 2% crude fiber.
Several studies of the short-term effects of dietary fiber on satiety have been conducted. In 2 studies,19,38 investigators measured postprandial satiety in dogs at 3 hours after feeding. They administered a restricted amount of food to adult dogs (approx 50 kcal/body weight0.75/d × body weight0.75); the diets contained 12.9 to 99.1 g of dietary fiber/1,000 kcal. Commercially available foods were provided 3 hours later, and intake and energy consumed for the commercial foods were used as a marker of satiety. Investigators determined that the food and energy intake for the 3-hour postprandial meal did not differ for the diets with different amounts of dietary fiber. Investigators in another study42 also used methods to evaluate postprandial satiety at 3 hours after feeding of dogs. In that study,42 they fed a high-fiber (97.9 g of dietary fiber/1,000 kcal) and high-protein diet or only a high-protein diet (55.9 g of total dietary fiber/1,000 kcal) by use of restricted feeding (33 kcal/body weight0.75/d × body weight0.75) in the morning, which was followed 3 hours later by provision of an unlimited amount of food. Their findings indicated that the high-fiber and highprotein diet significantly decreased energy intake at the 3-hour feeding. In that same study,42 postprandial satiety also was evaluated at 7 hours after feeding. Energy intake at 3 hours was significantly lower for the high-fiber and high-protein diet, compared with energy intake for the high-protein diet, but the effect was not detectable by 7 hours. Effects of dietary fiber supplementation on postprandial satiety at 6 hours were evaluated in Beagles.43 Those investigators compared effects for diets containing low fermentable fiber (8.5% cellulose in a diet) or high fermentable fiber (8.5% sugar beet pulp and 2% inulin in a diet) with effects for a diet not supplemented with fiber. Six hours after feeding those diets, they determined that the fiber-containing diets typically decreased food intake, compared with food intake for the diet that contained no fiber; however, the results were not significantly different among diets. Considering these results together, the effect of dietary fiber on satiety in dogs appears to provide very short-term (approx 3 hours) satiety but may not affect postprandial satiety at > 3 hours after feeding.
Weight loss is attributable to a decrease in energy intake as a consequence of dietary fiber supplementation. Because of inconsistent long-term satiety, effects of dietary fiber on weight loss are also inconclusive in dogs.19,38,41
Finally, it should be mentioned that the effect of dietary fiber on lipid metabolism in dogs has been sparsely studied. Thus, further research focusing on lipid metabolism is required to understand mechanisms of dietary fiber supplementation for counteracting obesity in dogs.
DAG
Diacylglycerol is an acylglycerol in which 2 fatty acids are esterified to sn-1 and -2 (1,2-DAG) or sn-1 and -3 (1,3-DAG) positions. By contrast, TAG consists of 3 fatty acids esterified to a glycerol backbone. In general, commercially available edible oils contain mainly TAG (87% to 98% of total acylglycerol). However, these oils also contain DAG as a minor component (0.8% to 9.5% of total acylglycerol; Table 1).44–46
Amounts of TAG and DAG in edible oils.
| Oil | TAG | DAG |
|---|---|---|
| Soybean44,45 | 97.9 | 1.0 |
| Palm44,45 | 93.1 | 5.8 |
| Cottonseed44,45 | 87.0 | 9.5 |
| Corn44,45 | 95.8 | 2.8 |
| Safflower44,45 | 96.0 | 2.1 |
| Olive44,45 | 93.3 | 5.5 |
| Rapeseed44,45 | 96.8 | 0.8 |
| Canola46 | 97.1 | 2.9 |
| Sesame seed46 | 95.2 | 4.1 |
Values reported are relative percentages.
Vegetable oils enriched with DAG (≥ 80% DAG, < 20% TAG, and < 2% MAG) were developed and have been commercially available in Japan since 1999 and in the United States since 2005.47 This DAG-enriched oil contains 1,2-DAG and 1,3-DAG in approximately a ratio of 3:7. Most characteristics of DAG, including palatability and digestibility, are similar to those of TAG. However, because of its unique chemical structure, DAG has been reported to beneficially affect lipid metabolism, plasma lipids, and adiposity. It should be mentioned that the effects of DAG appear to be a dose-dependent phenomenon; therefore, it may require that sufficient amounts of DAG be ingested for a beneficial effect to be observed.
Lipid metabolism of DAG—The metabolism of TAG and DAG oils in the intestinal lumen, mucosa, and lymph differs (Figure 1). During digestion, fat ingestion stimulates the secretion of cholecystokinin in the duodenum, which subsequently stimulates secretion of pancreatic lipase.48 When dietary TAG is ingested, it can be hydrolyzed by pancreatic lipase, which selectively hydrolyzes sn-1 and -3 positions of fatty acids to yield 2-MAG and 2 free fatty acids. Because pancreatic lipase is highly active, nearly all dietary TAG is hydrolyzed under physiologic conditions. The free fatty acids and 2-MAG then form micelles with bile acids, which are subsequently absorbed into intestinal mucosal cells.48 In enterocytes, TAG is reesterified via the 2-MAG pathway in which 1,2-DAG (or 2,3-DAG) is formed from 2-MAG and 1 free fatty acid via MAG acyltransferase.49 Then, TAG is produced from 1,2-DAG (or 2,3-DAG) and a free fatty acid via DGAT. The reesterified TAG is incorporated into chylomicrons by microsomal triglyceride transfer protein and then secreted into the bloodstream via the lymphatic system.48
Illustration depicting TAG and DAG metabolism in the intestinal lumen and mucosal cells and chylomicron formation. Notice that DAG ingestion and metabolism results in a decrease in postprandial triglyceride contents, compared with TAG ingestion and metabolism. MGAT = Monoacylglycerol acyltransferase. OH = Hydroxyl group. OPO32− = Phosphate group.
Citation: Journal of the American Veterinary Medical Association 235, 11; 10.2460/javma.235.11.1292
Illustration depicting TAG and DAG metabolism in the intestinal lumen and mucosal cells and chylomicron formation. Notice that DAG ingestion and metabolism results in a decrease in postprandial triglyceride contents, compared with TAG ingestion and metabolism. MGAT = Monoacylglycerol acyltransferase. OH = Hydroxyl group. OPO32− = Phosphate group.
Citation: Journal of the American Veterinary Medical Association 235, 11; 10.2460/javma.235.11.1292
Illustration depicting TAG and DAG metabolism in the intestinal lumen and mucosal cells and chylomicron formation. Notice that DAG ingestion and metabolism results in a decrease in postprandial triglyceride contents, compared with TAG ingestion and metabolism. MGAT = Monoacylglycerol acyltransferase. OH = Hydroxyl group. OPO32− = Phosphate group.
Citation: Journal of the American Veterinary Medical Association 235, 11; 10.2460/javma.235.11.1292
Compared with TAG, dietary DAG contains 1,2-DAG and 1,3-DAG. Hence, 1,2-DAG is hydrolyzed to 2-MAG and 1 fatty acid by pancreatic lipase, which will then use the 2-MAG pathway in the intestinal mucosa for resynthesis of TAG. By contrast, 1,3-DAG is hydrolyzed to a fatty acid and 1-MAG (or 3-MAG), some of which may be further hydrolyzed to glycerol and a fatty acid by pancreatic lipase.50 In enterocytes, a small amount of 1-MAG (or 3-MAG) also appears to be converted to 1,3-DAG.51 However, both 1-MAG (or 3-MAG) and 1,3-DAG have little affinity as a substrate for MAG acyltransferase and DGAT and thereby are unable to be used in the 2-MAG pathway.52,53 Instead, 1-MAG (or 3-MAG) and 1,3-DAG are metabolized via the G3P pathway. This pathway is considered to be a much slower pathway than the 2-MAG pathway for several reasons. First, the enzymes catalyzing the 2-MAG pathway have a rate of reaction (ie, Michaelis-Menten constant) that is 0.01 times lower for the substrates, compared with that for the substrates of the G3P pathway. Second, the presence of 2-MAG in intestinal mucosal cells inhibits the G3P pathway. Finally, TAG formed by the G3P pathway is stored in the enterocyte cytosol, which is believed to be a slow-turnover pool.49,54 Therefore, a slow process of reesterification of TAG by the G3P pathway is believed to delay TAG secretion into the lymphatics and bloodstream.
The proposed hypothesis that administration of oil containing 1,3-DAG would delay or reduce TAG secretion into the circulation was investigated.55 Male Sprague-Dawley rats had a cannula and a catheter inserted into the thoracic duct and stomach, respectively, and were administered radiolabeled DAG or TAG into the stomach via the catheter. The 24-hour radioactivity recovery in the thoracic duct was then monitored. In the first hour after oil administration, recovery of radioactivity in the DAG-administered rats was nearly half that for the TAG-administered rats. In addition, plasma TAG concentration was significantly lower in the DAG group than in the TAG group. This reduction in radioactivity by DAG was still evident at 24 hours after oil administration. These results suggested that DAG ingestion delayed TAG secretion into the circulation for at least 24 hours after administration, and this reduction would therefore affect plasma TAG concentrations.55
Effects on chylomicron metabolism—In a recent study,56 investigators detected a small but significant increase in DAG concentration in chylomicrons of mice that ingested 20 wt% DAG, compared with results for mice that ingested 20 wt% TAG. It was postulated that an increase of DAG incorporation into chylomicrons may have acted to modify the chylomicron oil-water interface and thereby promote acylglycerol hydrolysis. There was also an increase in LPL activity for chylomicrons obtained from mice fed DAG or a lipid emulsion mixed with DAG as substrate. Thus, it may be concluded that the hypolipidemic effect of DAG is derived from increased LPL-mediated lipolysis of acylglycerols in chylomicrons. Results of another study57 in Sprague-Dawley rats also support a decrease in plasma TAG concentrations as a consequence of enhanced LPL activity in adipose tissue following DAG intake. Therefore, it appears that DAG-enriched chylomicrons are likely to stimulate LPL activity in the postprandial period. However, it remains to be established whether increased LPL activity is the reason for the decrease in plasma TAG concentrations. For example, a study58 in cats revealed that LPL-deficient male cats fed a diet containing 10 wt% DAG did not have a decrease in postprandial plasma TAG concentrations, compared with results for cats fed a diet containing 10 wt% TAG. By contrast, a study59 in humans revealed that when individuals homozygous for the LPL gene deletion consumed DAG oil, postprandial plasma TAG concentrations were still decreased, compared with results after ingestion of TAG oil. Moreover, DAG ingestion reduced plasma TAG concentrations, compared with results for TAG ingestion in a human deficient in apo CII, which is a cofactor of LPL.51 These results suggest that LPL activity may help reduce plasma TAG concentrations; however, the hypolipidemic effect of DAG may be independent of LPL-mediated lipolysis.
Effects on plasma lipids—In support of the aforementioned observations, investigators in 1 study60 detected a significant reduction in plasma TAG concentrations in rats fed > 5 wt% DAG (instead of being fed TAG) as a fat source. Investigators in another study61 also reported a hypolipidemic effect of DAG. In that study,61 clinically normal men were administered different doses (10, 20, or 44 g) of DAG oil or TAG oil for 7 days. Postprandial serum TAG concentration was significantly decreased at 4 and 6 hours for the DAG oil group, compared with the concentration for the TAG oil group; the effect was independent of the dose administered. When plasma lipoprotein fractions (ie, VLDL, LDL, and HDL) and chylomicrons were evaluated at 4 and 6 hours in humans administered 20 g of DAG or TAG, the TAG concentrations in chylomicrons, VLDL, and LDL, but not HDL, were lower in the DAG group than in the TAG group. In addition, the investigators determined that the HDL concentration was increased by DAG ingestion, compared with the concentration for TAG ingestion. Therefore, it appears that DAG improves postprandial hypertriglyceridemia and also decreases the ratio of LDL:HDL, which is one of the risk factors for development of atherosclerosis.
Effects on obesity management—Long-term feeding of DAG can have an effect on reducing excessive body fat as well as TAG concentrations. Although the mechanism involved is not fully understood, enhancement of genes in the fatty acid oxidation pathway may be a factor to consider in long-term DAG ingestion. For example, investigators in 1 study62 detected less body weight gain when C57BL/KsJ-db/db mice (ie, leptinsignaling–deficient mice) were fed a DAG diet containing 4% α-linolenic for 1 month, compared with body weight gain for mice fed a TAG diet containing 4% α-linolenic. The group consuming the DAG-containing diet had upregulation of acyl-CoA oxidase, mediumchain acyl-CoA dehydrogenase, fatty acid binding protein, and uncoupling protein-2 mRNA expression and BHB activity in the small intestines and an increase in rectal temperature. However, gene expressions related to fat oxidation in the liver were unchanged as a result of oil type.62 In another study,63 Sprague-Dawley rats were fed 20 wt% DAG or 20 wt% TAG diets for 8 weeks. Results revealed a significant reduction of body weight gain in the DAG group, compared with that for the TAG group, at week 8 despite the same food intake for both diets. The reduction in body weight gain for DAG ingestion was associated with a reduction of abdominal (mesenteric, perirenal, and epididymal) body fat. At the same time, upregulation of acyl-CoA carnitine acyltransferase and downregulation of DGAT were detected in the liver as a consequence of DAG ingestion. Acyl-CoA carnitine acyltransferase is an enzyme that provides substrate for fat oxidation, whereas DGAT is a pivotal enzyme for TAG biosynthesis in the liver and provides TAG in peripheral tissues via VLDL. Thus, it was concluded that body fat reduction was attributable to changes in enzyme regulation. In addition, an increase in enzymes related to β-oxidation, such as carnitine palmitoyltransferase, acyl-CoA dehydrogenase, acyl-CoA oxidase, 2,4-dienoyl-CoA reductase, and Δ3,Δ2-enoyl-CoA isomerase, was detected in the liver when 65.8 and 93.9 g of DAG/kg of diet was fed to rats for 21 days.64
Studies in humans and rodents—To determine whether the effect of DAG on weight reduction also applies to humans, overweight and obese men and women were given 8 to 9 g of DAG oil or TAG oil in a hypocaloric diet for 6 months.65 Results revealed that the DAG group had a significant decrease in body weight and fat mass, compared with the outcome for the TAG group. Other studies in humans also consistently revealed a reduction in body composition as a consequence of longterm ingestion of DAG. In 1 study,66 investigators provided healthy men with DAG oil or TAG oil (10 g/d) as part of their diet for 16 weeks. At the end of the study, both diet groups lost body weight but the DAG group lost a greater amount of body weight than did the TAG group. In addition, at week 16, total fat and visceral fat determined by use of computed tomography was significantly reduced in the DAG group, compared with results for the TAG group. Moreover, when C57BL/6J mice (ie, obesity-prone mice) were fed diets containing 30 wt% TAG or 30 wt% DAG for 5 months, the DAG group had a significant decrease in body weight gain and visceral fat, compared with results for the TAG group. Moreover, the decrease was associated with a decrease in circulating leptin concentrations, which is an indicator of an early period of obesity development.67 In a similar study in mice,62 investigators reduced the oil amount to 15 wt% DAG or 15 wt% TAG and fed the diets for 8 months; results revealed accumulation of significantly less body fat in the mice fed the DAG diet than in the mice fed the TAG diet.
Studies in dogs—Only a few studies have been published on the effects of DAG on hypolipidemia and weight loss in dogs. In 1 study,68 investigators fed overweight (body condition score ≥ 4/5) adult Beagles 7% DAG oil or 7% TAG oil coated on a dry, extruded diet for 6 weeks. Both diets were isocaloric and had similar nutrient contents, fatty acid compositions, and digestibilities. The diets were fed at an amount intended to maintain the overweight condition of the dogs during the study. Results revealed that both groups consumed the same amount of energy; however, only the DAG oil group had a significant decrease from baseline values of body weight and body fat. In addition, weight loss was significantly greater in the DAG oil group than in the TAG oil group. One possible explanation for these findings is that the DAG oil group had a significant increase in fasting serum BHB concentration at week 6, compared with the concentration at week 1. In addition to the effect of DAG on weight loss, the investigators detected a hypolipidemic effect in dogs, including lower fasting serum TAG and total cholesterol concentrations in the DAG oil group at week 6.68 Additional studies will help to better define the effect of DAG on weight loss in dogs.
Safety—The safety of chronic ingestion of DAG has been evaluated in humans,69 rodents,70,71 and dogs.72 In these studies, investigators did not detect any safety issues after the consumption of DAG. In dogs, toxic effects for chronic dietary intake of DAG (up to 9.5% in a diet) were investigated.72 After ingestion of DAG for 1 year, clinical condition; food consumption; results for hematologic analysis, urinalysis, serum biochemical analysis, ECG examination, and histologic examination; and changes in organ weights were not different from those after TAG ingestion. Although additional research is expected to elucidate longer-term (> 1 year) safety for DAG ingestion, current findings support the possible use of DAG as an ingredient that could be included for weight management purposes in foods formulated for dogs.
LGI Starch
Glycemic index is defined as the area under the glucose response curve to a carbohydrate-containing food, compared with the response to a specific amount of white bread.73 Thus, the GI concept allows comparison of the glucose response to various foods. The GI value of a food relates to the rate of digestion of a food, which is affected by macronutrient interactions, gastric emptying rate, food form, cooking, particle size, and dietary fibers but not by soluble fiber.74–76 The GI value also strongly correlates among starch types.77
Starch is a term that refers to a type of carbohydrate that is composed of linear chains of glucose polymer (ie, amylose) or highly branched chains of glucose polymer (ie, amylopectin).78,79 Both amylose and amylopectin are hydrolyzed by amylase to release glucose, which may be absorbed into intestinal enterocytes. However, hydrolysis of amylose is slower than that of amylopectin because of structural differences. Consequently, amylose starch results in a lower glucose response and therefore is considered to be an LGI, compared with amylopectin starch. Thus, LGI foods provide a slower and more consistent source of glucose to the bloodstream, thereby stimulating less insulin release than for HGI foods.80 Because insulin stimulates lipogenesis and inhibits lipolysis, it is theoretically possible that more weight loss may be obtained with longer-term ingestion of LGI foods, compared with that for HGI foods, in part by changing lipid metabolism.81,82 Although the ingestion of diets containing mixed starch types may minimize a beneficial effect, this concept of the use of LGI foods for obesity management is established in human nutrition.
Studies in humans and rodents—Clinically normal or diabetic Sprague-Dawley rats were fed diets (575 g/kg) containing LGI starch (waxy corn starch) or HGI starch (mung bean starch) for 3 weeks to evaluate the GI effect on lipid metabolism.83 At week 3, body weight, body fat, plasma triglyceride concentration, and LPL activity were not different between the LGI diet and HGI diet groups. However, clinically normal rats had greater activity of fatty acid synthase and greater gene expression in epidydymal adipose tissue in the HGI diet group than in the LGI diet group. In addition, the content of insulin-regulated glucose transporter-4 was increased in adipose tissue of clinically normal rats fed the HGI diet, compared with results for rats fed the LGI diet. Moreover, activity of phosphoenolpyruvate carboxykinase, which is an enzyme regulated by insulin and is a key enzyme for gluconeogenesis, was significantly decreased in the liver of both clinically normal and diabetic rats fed the HGI diet. Thus, these results suggested that HGI starch stimulates activity of fatty acyl synthase and lipogenesis and may thereby provide undesirable long-term metabolic effects, compared with those for LGI starch.83
In 1 study,84 male Sprague-Dawley rats that had part of the pancreas removed were given diets that contained LGI (60% amylose and 40% amylopectin) or HGI (100% amylopectin) at the rate of 542 g/kg for 18 weeks. Food intake was adjusted to maintain the same body weight between the diet groups during the study. It was determined that rats fed the HGI diet needed to have their food intake restricted after 8 weeks to maintain body weight. Consequently, at week 18, the cumulative food intake of the LGI diet group was 13% greater than that of the HGI diet group. The LGI diet group had a lower amount of body fat and fasting plasma triglyceride concentrations and a higher lean body mass than did the HGI diet group.84
In humans, the beneficial effects of LGI on obesity management remain controversial because of variations in selection of GI and carbohydrate sources in diets. However, results of some studies85–89 support an LGI effect. For example, investigators in 1 study85 evaluated the GI effect on lipid metabolism as well as weight reduction. In that study, 11 healthy adult men were offered an LGI- or HGI-containing diet twice a day (breakfast and lunch) for 5 weeks in a crossover design (mean GI; 74% vs 39.5% for the HGI and LGI diets, respectively). At the end of the study, they determined that the LGI diet lowered postprandial plasma glucose and insulin concentrations, compared with results for the HGI diet. Moreover, although a reduction in body weight was not detected as a function of diet, the LGI diet group had a significant decrease in total body fat, compared with that for the HGI diet group, and this finding was associated with a decrease in leptin, LPL, and hormonesensitive lipase mRNA concentrations in subcutaneous abdominal adipose tissues. In another study,86 38 overweight, nondiabetic men and women were offered LGI or HGI starch (mean GI; < 50 for LGI vs > 70 for HGI) ad libitum for 5 weeks. At the end of the study, body weight had decreased significantly in the LGI group, compared with results for the HGI group. The LGI diet also caused an improvement in lipid profiles, including a decrease in total cholesterol and LDL concentrations and the ratio of LDL:HDL, whereas these variables were not altered by the HGI diet.
Studies in dogs—To our knowledge, no studies have been conducted to evaluate the GI concept on obesity management of dogs. With regard to the glycemic response after LGI administration to dogs, investigators in 1 study90 determined that the amount of starch in commercially available diets for dogs is the major determinant of the glucose and insulin responses of healthy adult dogs. This finding is consistent with findings in the aforementioned studies in humans and rodents. Because starch type may be more carefully controlled in dogs than it is in humans, the benefits of LGI starch may be more readily detected. Therefore, introduction of the LGI concept in foods formulated for dogs may be of benefit in efficient and healthy weight reduction.
Combination Effects of DAG and LGI in Dogs
The effect of a single meal containing DAG on lipid metabolism has been reported.91 In that study, 12 clinically normal and sexually intact female adult Beagles were used with a 4 × 4 Latin square design. Dogs were fed one of the following diet combinations: DAG-LGI, DAG-HGI, TAG-LGI, or TAG-HGI. High-amylose corn starch and waxy corn starch were used as a source of LGI and HGI, respectively. Nutrient composition of these diets (calculated on a metabolizable-energy basis) was 16.5% protein, 25.3% carbohydrate, and 58.3% fat. A DAG effect was observed in which there was a significant decrease of peak values and duration for postprandial plasma TAG concentrations at 2 and 3 hours after ingestion of the DAG-containing diets, although plasma BHB concentrations were unchanged among the diets. An LGI effect was also observed in which postprandial plasma insulin concentrations were significantly suppressed after ingestion of the LGI-containing diets. Plasma lipase activities did not differ significantly among the diets; the LGI-containing diet caused a slight but nonsignificant (P = 0.085) increase in hepatic lipase activity. Considered together, these results suggested that the DAG-LGI combination diet may possibly improve the postprandial lipid profile after ingestion of a single meal. The data also lent credence to the possibility that longer-term effects of this DAG-LGI combination may provide additional metabolic alterations regarding lipid metabolism and obesity management.
To elucidate this possibility, the longer-term effect of DAG was evaluated by use of the same diet combinations, which were fed to obese adult female Beagles for 9 weeks in an amount needed to maintain obese body weights.b,c All dogs lost body weight during the study because they typically consumed only 68% of the food offered. However, the LGI diet groups lost a higher percentage of body weight (2%) overall than did the HGI groups (1%). This difference appeared to be attributable to the fact that the LGI diets contained 12% less metabolizable energy than did the HGI diets. Plasma insulin concentrations were significantly lower in the LGI groups, compared with concentrations in the HGI groups, and nonesterified fatty acid concentrations were also increased with the LGI diets. The DAG effects observed included a decrease in postprandial plasma triglyceride concentrations at weeks 1 and 8 and an increase in BHB concentrations at week 8, compared with concentrations for the TAG diets. These findings support the possibility that less triglyceride enters the bloodstream after eating (ie, a DAG effect), with an increase in the relative amounts of nonesterified fatty acids made available in a lower insulin environment (ie, LGI effects).
Conclusion
Modification of lipid metabolism via the use of various fiber types, LGI starch, and DAG-enriched oils may provide an effective yet safe means for managing weight loss in obese dogs. Each of these diet components has shown promise in the management of this important medical condition via their potentially beneficial effects on satiety and energy metabolism and utilization. Although dietary fiber may provide between-meal satiety during dieting, the inclusion of LGI starch can mitigate the insulin response and provide lower digestibility, compared with the responses for HGI starch. The use of DAG-enriched oils as a dietary fat source has the potential to reduce postprandial hypertriglyceridemia and increase fatty acid oxidation to help mitigate adipose accumulation in tissues during weight reduction. The use of these dietary components in carefully conducted studies in dogs and cats will provide new insights and guidance for their use in companion animals.
ABBREVIATIONS
| BHB | β-Hyroxybutyrate |
| DAG | Diacylglycerol |
| DGAT | Diacylglycerol acyltransferase |
| GI | Glycemic index |
| G3P | Glycerol 3-phosphate |
| HDL | High-density lipoprotein |
| HGI | High glycemic index |
| LDL | Low-density lipoprotein |
| LGI | Low glycemic index |
| LPL | Lipoprotein lipase |
| MAG | Monoacylglycerol |
| TAG | Triacylglycerol |
| VLDL | Very low-density lipoprotein |
| wt% | Weight percentage |
Okawa M, Ban T, Umeda T, et al. Investigation of percent body fat in dogs visiting veterinary practices in Japan (abstr). J Vet Intern Med 2007;21:656.
Mitsuhashi Y, Nagaoka D, Bigley K, et al. Lipid metabolism in obese beagles during weight loss fed low glycemic index starch and diacylglycerol diets (abstr). J Vet Intern Med 2007;21:656–657.
Nagaoka D, Mitsuhashi Y, Bigley K, et al. Low glycemic index carbohydrate and diacylglycerol diet promotes more efficient weight loss, improves insulin control, and modifies post-prandial non-esterified fatty acid response in obese dogs (abstr). J Vet Intern Med 2007;21:605.
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