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Asad Saeed

Publications and source records attributed to Asad Saeed.

2 recordsLinked to original sources

The metabolic response of subjects with type 2 diabetes to a high-protein, weight-maintenance diet.

In a randomized, crossover 5-wk study design, we recently reported that a weight-maintaining diet in which the percentage of total food energy as protein was increased from 15-30% resulted in a decrease in postprandial glucose and glycohemoglobin in people with untreated type 2 diabetes without a significant change in insulin. Protein was substituted for carbohydrate in the diet. The fat content remained unchanged. In this publication, we present data on other hormones and metabolites that were considered to potentially be affected by substitution of protein for carbohydrate in the diet. The mean fasting plasma GH and total IGF-I concentrations were elevated on the 30% protein diet. The urinary free cortisol also was increased. However, the urinary aldosterone was unchanged. Although urinary pH was decreased, calcium excretion was not significantly increased. The plasma postprandial alpha-amino nitrogen concentrations were increased, but the 24-h integrated concentration was unchanged, indicating an accelerated amino acid removal rate. The plasma urea nitrogen was increased as expected. The urea production rate also was increased such that a new steady-state fasting value was present. The calculated urea production rate accounted for 97% of the protein ingested on the 15% protein diet, but only 80% on the 30% protein diet, suggesting net nitrogen retention on the high-protein diet. In conclusion, an increase in dietary protein results in a number of metabolic adaptations in addition to reducing the circulating glucose concentration. Serum TSH, total T(3), free T(4), B(12), folate, homocysteine, uric acid, and creatinine concentrations were unchanged.

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A fasting-induced decrease in plasma glucose concentration does not affect the insulin response to ingested protein in people with type 2 diabetes.

We previously have reported that protein, on a weight basis, is just as potent as glucose in increasing the insulin concentration in people with type 2 diabetes. In people without diabetes, protein is only approximately 30% as potent as glucose in this regard. In the present study, we tested the hypothesis that the increased insulin responsiveness to protein in people with type 2 diabetes is due to the elevated plasma glucose concentration in these individuals. Seven male subjects with untreated type 2 diabetes were given 50 g protein in the form of very lean beef at 8 AM after an overnight fast. On another occasion, the same individuals were fasted for an additional 24 hours to lower their plasma glucose concentration to near the normal reference range. They were then given 50 g protein. The 8 AM glucose concentration was lower after 24 hours of additional fasting, as expected. After ingestion of the protein meal, there was an unexpected, modest increase in glucose concentration after an additional 24 hours of fasting that was not observed with only an overnight fast. Despite the approximately 15% lower plasma glucose concentration at the time of the protein meal, the insulin responses were nearly identical. Thus, the greater insulin response to ingested protein is not likely to be due merely to a higher initial glucose concentration.

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