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Defeat the effects of a slow metabolism by reducing caloric and carbohydrate intake
The results from our continued research efforts explain why the slow metabolism of obese individuals does not oxidize glucose to energy. Unfortunately, obese individuals convert most of the glucose to fat following the ingestion of carbohydrate rich meals. It is concluded from the findings in figure 2 (below) that an obese individual's slow metabolism does not oxidize glucose efficiently because the release of trypsin from the exocrine portion of the pancreas is not synchronized with the release of insulin from the endocrine portion of the pancreas.
Why is it so important that the release of trypsin from the exocrine portion of the pancreas occur simultaneously with the release of insulin from the endocrine portion of the pancreas?
Answer: Insulin is the principal hormone that controls the metabolism of carbohydrates. Insulin is produced by the endocrine portion of the pancreas. The major function of insulin is to facilitate the uptake of glucose by body cells. However, in order for insulin to do its job, it requires the action of the trypsin enzyme.
Insulin is classified as a prohormone. A prohormone is the inactive form of a hormone. Insulin is initially secreted in its inactive form by the endocrine portion of the pancreas in response to the ingestion of carbohydrate rich meals. The inactive form of insulin is called proinsulin. Proinsulin consists of two polypeptide chains, the A- chain and the B- chain. The connecting peptide forms a link between the two chains. Before proinsulin (inactive form)
can be converted to insulin (active form), the connecting peptide has to be cleaved (removed).
In adddition, glucose cannot be taken up by the cells unless proinsulin has been converted to active insulin. Proinsulin lacks the capacity to facilitate the uptake of glucose by the cells. Only active insulin can facilitate the uptake of glucose by cells.
Trypsin is a proteolytic enzyme (an enzyme that acts on proteins). Trypsin is produced by the exocrine portion of the pancreas. Trypsin plays a very important role in the cleavage of the C-peptide from proinsulin, thereby converting proinsulin to active insulin.
Figure 2 clearly shows that obese individuals produce trypsin from the pancreas, but not at the same time as proinsulin (inactive form of insulin) is secreted from the endocrine portion of the pancreas. After close examination, it is obvious that the defect of a slow metabolism of carbohydrates by obese individuals appears to be due to the delayed release of trypsin from the exocrine portion of the pancreas.
It appears that there is a crucial time period for the activation of insulin following the ingestion of carbohydrate rich meals. It is inferred from the composite graph (figure 2) that the conversion of proinsulin to insulin takes place within thirty minutes following the ingestion of a carbohydrate load by thin individuals.
It is also inferred from the composite graph (figure 2) that the conversion of proinsulin to insulin takes place three hours after the ingestion of a carbohydrate load by
But in order for glucose to be completely oxidized (burned) to energy, the bulk of the glucose must be taken up by skeletal muscle cells within thirty minutes following the ingestion of carbohydrate rich meals.
Skeletal muscle constitutes over 75% of the body's total mass. It is within this very large skeletal muscle compartment of the human body where billions of glucose molecules must be trapped within thirty minutes following the ingestion of a carbohydrate rich meal to be oxidized to energy. Glucose is oxidized via a specific metabolic
pathway in skeletal muscle cells called glycolysis. The glucose that enters into the skeletal muscle cells is completely oxidized to carbon dioxide, water and energy (ATP), none being converted to fat.
Just think about it for a moment ... all of the glucose from a single carbohydrate rich meal has to be taken up by skeletal muscle cells within thirty minutes after it is ingested or it does not get converted to energy, but to fat. Just imagine what can happen to an individual who has a slow metabolism of carbohydrates, and who indulges in 4 to 6 carbohydrate rich meals per day for several months... they will end up becoming morbidly obese.
The big question is how can a slow metabolism be treated. Unfortunately, there is no medicine presently available to treat the defect (delayed release of trypsin from the pancreas following the ingestion of carbohydrate rich meals). However, one can limit the amount of carbohydrates ingested through a low calorie, low carb diet plan to compensate for thier slow metabolism of glucose.
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