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Nutrition & Product Information
Diabetes Mellitus & Dairy Food Consumption
Nutrient-Gene Interactions in Diabetes — A Case for Intervention
As pointed out above, diabetes is often associated with obesity. Thus, it should come as no surprise that intervention strategies that target obesity will have an effect on the time course of diabetes development. Marshall et al. (69) studied 134 subjects with impaired glucose tolerance. Those subjects consuming 40.6% of their intake energy as fat were less likely to proceed on to type 2 diabetes than those subjects consuming 43.4% of their daily energy intake as fat. This was not a feeding study but was simply a study of what people ate and their progression towards diabetes. The difference in fat intake (~3%) was quite small yet these authors showed that the level of fat consumption significantly affected diabetes risk even after correcting for obesity and markers for abnormal glucose metabolism. The implication is that the fat intake can significantly affect the time course for diabetes development.
In another population study using 12,700 participants without evidence of diabetes, serum magnesium levels were inversely correlated with fasting serum insulin, plasma glucose, plasma high density lipoproteins and diastolic and systolic blood pressure. (70) These findings were similar to those reported by Humphries et al. (71) and Rosolova. (72)
Suggesting that since dairy foods provide so much magnesium (~16% of the daily magnesium intake) these foods would be beneficial with respect to insulin action and glucose homeostasis.
Kumar et al. have reviewed the literature on the prevention of type 2 diabetes. (73) From the diet perspective, reduction in the conversion of impaired glucose tolerance to type 2 diabetes was reduced from 29% to 13% in Swedish subjects through the limitation of energy intake from carbohydrates and fats. (74) Similar results were obtained in another study also conducted in Sweden. (75) In this second study, subjects were instructed in diet choices as well as in an exercise protocol. Annual assessments of the subjects showed that over the six years of the study the rate of conversion from glucose intolerance to type 2 diabetes was reduced 50%. A number of studies all directed towards increasing physical activity and reducing body fatness have shown that it is possible to intervene with the process of diabetes development where it is associated with excess fat stores or obesity. Table 8 provides a summary of some of these studies.
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Table 8.
Some Intervention Studies |
| |
| Investigators |
Subjects/Origin |
Study Length |
Intervention/Outcome |
|
| O’Dea (76) |
Aus. Aborigines |
7 weeks |
Reversion to trad. lifestyle/tolerance |
| Sartor et al. (74) |
Swedish adults |
10 years |
Reduced energy intake/Reduced conversion to diabetes |
| Ericsson et al. (75) |
Swedish adults |
6 years |
Reduced energy intake, increased exercise/reduced conversion to diabetes |
| Viswanathan et al. (77) |
Offspring of diabetic parents |
4 years |
Weight control & exercise/diabetes onset delayed |
| Ericsson et al. (78) |
Overweight adults |
1 year |
Weight control, lifestyle advice/Weight loss, no effect on diabetes |
| Pan et al. (79) |
Chinese adults |
6 years |
Diet advise &/or exercise /Weight loss & diabetes delay |
|
King and Daniel as well as Stern and Melander have also reviewed the literature on intervention or prevention of diabetes. (80-82) They suggest that not only should clinicians focus on the reduction in body fat stores but also pay attention to the various risk factors for cardiovascular disease. As noted in the introduction on the prevalence of diabetes, people with diabetes have five times the risk of developing cardiovascular disease as people without diabetes. Hence, intervention strategies should also include those tactics that will reduce the likelihood of a cardiovascular event. In view of the observation that obesity is occuring in children and adolescents, it would appear that these age groups should be studied to determine if the interventions found successful in adults would be successful in children as well.
Several intervention trials have been conducted that addressed cardiovascular risk factors. The CATCH Multicenter Trial was a school based research study that had as its objective the effectiveness of changes in school lunches, physical education, smoking policy curricula and family activities. (83,84) The percent saturated fat and total fat was reduced in the diets of those subjects in the intervention group. Physical activity was also increased. This trial lasted 3 years and involved 5,016 third grade students. While the objectives of reducing fat intake and increasing physical activity were achieved, there were no significant differences between the control and intervention groups in blood pressure, body size, or blood cholesterol. In another study, the Heart Start Study, children in the third grade were again used and again the goal was to reduce dietary fat intake and increase physical activity. (82) This was achieved and again few differences in cardiovascular risk factors were noted in these children. As with the CATCH Trial, diabetes was not assessed but the hoped-for outcome was that in modifying diet and physical activity in the child, one could have an effect on that child as he/she matures. Habits adopted as a child might have a long-term effect on subsequent adult health behavior such that a delay in the development of heart disease and also diabetes might occur. Intervention studies per se in children with respect to type 2 diabetes have not been conducted primarily because this has not been a child health problem until recently. Now with the early onset of obesity these studies are needed.
Are there other strategies that could modify the phenotypic expression of a diabetes genotype? Feeding an egg based diet to BHE/Cdb rats having a diabetes genotype in the mitochondrial genome, resulted in a delay in the onset of impaired glucose tolerance. (86) Rats of this strain fed a 10% fat diet lived longer and had a delay in the development of diabetic renal disease when fed beef tallow, when compared to either corn oil or menhaden oil. Those fed the fish oil diet had the shortest life spans and early onset of renal lesions. (87) Longevity studies in humans with this kind of strict dietary regimens have not been conducted.
In humans with defects in insulin receptors, the logical strategy would be to reduce the glucose stimulated need for insulin bound to the fat cell, liver cell or muscle cell. Diets low in simple sugars and diets that maintain (or attain) ideal body weight should be used. This strategy would also be useful in those with mutations in the gene for glycogen synthesis. The objective would be to decrease the need to synthesize glycogen by keeping the carbohydrate intake relatively unrefined and low in amount. In persons having mutation(s) in the glucose transporters and in mutations in the mitochondrial genome, the strategy would be to increase the fluidity of the plasma and intracellular membranes. Such a strategy would maximize the activity of the insulin receptors through inducing a more fluid membrane. The receptors are membrane bound and their activity is dependent on the fluidity of the lipid in which they are embedded. Several studies have been conducted showing that dietary fat type will have this effect.
In diabetes-prone BHE/Cdb rats fed fish oil, insulin sensitivity was increased via an effect on glucose uptake by the fat cell. (88,89) The type of fat in the diet fed these rats affected glucose
homeostasis, insulin receptor number and binding activity and glucose uptake and oxidation. (88-91) Ryan et al. (92) showed that humans provided a Mediterranean diet had an improvement in their insulin sensitivity which these investigators attributed to a diet-induced change in membrane composition that in turn influenced membrane fluidity and function. The Mediterranean diet is rich in oleic acid. Oleic acid is a monounsaturated fatty acid (18:1). This fatty acid is one of the most common fatty acids found in dairy fat. Thus, if a Mediterranean diet could have this effect, there is no doubt that ingestion of dairy fat would have the same effect. The mole percent of oleic acid in dairy fat is about ~26.5%. The only fatty acid in greater concentration in dairy fat is palmitic acid (16:0) at ~29 mole percent. (93)
Where there are mutations in the gluconeogenic pathway, the strategy would be to avoid prolonged periods without food necessitating the upregulation of gluconeogenesis that in turn contributes glucose to the circulation in excess. In this scenario the problem is not in the gluconeogenic pathway itself but in the factors that control it. Upregulation is a common feature in diabetes and part of the problem in glucose homeostasis management is the down regulation of this pathway. Several of the oral hypoglycemic drugs recently developed have this as their pharmaceutic objective.
For those patients with diabetes due to mutations in the MODY genes, the diet prescriptions might be different. These people might need to increase their fat intake to gain better control of their glucose metabolism. This may also be true for those who develop diabetes due to an error in the mitochondrial genome.
Increasing physical activity would potentiate the diet strategies in most of the people with genotypes that phenotype as diabetes because it would not only increase energy expenditure but would also increase the non-insulin dependent use of glucose by the muscles. This is not a good strategy with respect to those afflicted with mutations in the mitochondrial genome. These persons usually are unable to sustain significant muscle activity because the mutations result in malfunctioning mitochondria that are needed for muscular activity.
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