The first organ to receive glucose, fructose, and galactose is the liver. The liver takes them up and converts galactose to glucose, breaks fructose into even smaller carbon-containing units, and either stores glucose as glycogen or exports it back to the blood. How much glucose the liver exports to the blood is under hormonal control and you will soon discover that even the glucose itself regulates its concentrations in the blood.
Glucose levels in the blood are tightly controlled, as having either too much or too little glucose in the blood can have health consequences. Glucose regulates its levels in the blood via a process called negative feedback. An everyday example of negative feedback is in your oven because it contains a thermostat. The glucose thermostat is located within the cells of the pancreas. After eating a meal containing carbohydrates glucose levels rise in the blood.
Insulin-secreting cells in the pancreas sense the increase in blood glucose and release the hormone, insulin, into the blood. In the case of muscle tissue and the liver, insulin sends the biological message to store glucose away as glycogen. The presence of insulin in the blood signifies to the body that glucose is available for fuel. As glucose is transported into the cells around the body, the blood glucose levels decrease.
Insulin has an opposing hormone called glucagon. Glucagon-secreting cells in the pancreas sense the drop in glucose and, in response, release glucagon into the blood.
Glucagon communicates to the cells in the body to stop using all the glucose. More specifically, it signals the liver to break down glycogen and release the stored glucose into the blood, so that glucose levels stay within the target range and all cells get the needed fuel to function properly. Almost all of the carbohydrates, except for dietary fiber and resistant starches, are efficiently digested and absorbed into the body.
Some of the remaining indigestible carbohydrates are broken down by enzymes released by bacteria in the large intestine. The products of bacterial digestion of these slow-releasing carbohydrates are short-chain fatty acids and some gases.
The short-chain fatty acids are either used by the bacteria to make energy and grow, are eliminated in the feces, or are absorbed into cells of the colon, with a small amount being transported to the liver. Colonic cells use the short-chain fatty acids to support some of their functions. The liver can also metabolize the short-chain fatty acids into cellular energy. The yield of energy from dietary fiber is about 2 kilocalories per gram for humans, but is highly dependent upon the fiber type, with soluble fibers and resistant starches yielding more energy than insoluble fibers.
Since dietary fiber is digested much less in the gastrointestinal tract than other carbohydrate types simple sugars, many starches the rise in blood glucose after eating them is less, and slower.
These physiological attributes of high-fiber foods i. Less than an hour later you top it off with a slice of haupia pie and then lie down on the couch to watch TV. Insulin sends out the physiological message that glucose is abundant in the blood, so that cells can absorb it and either use it or store it. The result of this hormone message is maximization of glycogen stores and all the excess glucose, protein, and lipids are stored as fat.
A typical American Thanksgiving meal contains many foods that are dense in carbohydrates, with the majority of those being simple sugars and starches. These types of carbohydrate foods are rapidly digested and absorbed. After eating a meal containing carbohydrates glucose levels rise in the blood.
Insulin-secreting cells in the pancreas sense the increase in blood glucose and release the hormone, insulin, into the blood. In the case of muscle tissue and the liver, insulin sends the biological message to store glucose away as glycogen.
The presence of insulin in the blood signifies to the body that glucose is available for fuel. As glucose is transported into the cells around the body, the blood glucose levels decrease. Insulin has an opposing hormone called glucagon. Glucagon-secreting cells in the pancreas sense the drop in glucose and, in response, release glucagon into the blood. Glucagon communicates to the cells in the body to stop using all the glucose. More specifically, it signals the liver to break down glycogen and release the stored glucose into the blood, so that glucose levels stay within the target range and all cells get the needed fuel to function properly.
Almost all of the carbohydrates, except for dietary fiber and resistant starches, are efficiently digested and absorbed into the body. Some of the remaining indigestible carbohydrates are broken down by enzymes released by bacteria in the large intestine. The products of bacterial digestion of these slow-releasing carbohydrates are short-chain fatty acids and some gases. The short-chain fatty acids are either used by the bacteria to make energy and grow, are eliminated in the feces, or are absorbed into cells of the colon, with a small amount being transported to the liver.
Colonic cells use the short-chain fatty acids to support some of their functions. The liver can also metabolize the short-chain fatty acids into cellular energy. The yield of energy from dietary fiber is about 2 kilocalories per gram for humans, but is highly dependent upon the fiber type, with soluble fibers and resistant starches yielding more energy than insoluble fibers.
Since dietary fiber is digested much less in the gastrointestinal tract than other carbohydrate types simple sugars, many starches the rise in blood glucose after eating them is less, and slower. These physiological attributes of high-fiber foods i. Less than an hour later you top it off with a slice of haupia pie and then lie down on the couch to watch TV.
Insulin sends out the physiological message that glucose is abundant in the blood, so that cells can absorb it and either use it or store it.
The result of this hormone message is maximization of glycogen stores and all the excess glucose, protein, and lipids are stored as fat. A typical American Thanksgiving meal contains many foods that are dense in carbohydrates, with the majority of those being simple sugars and starches. These types of carbohydrate foods are rapidly digested and absorbed. Blood glucose levels rise quickly causing a spike in insulin levels. Contrastingly, foods containing high amounts of fiber are like time-release capsules of sugar.
A measurement of the effects of a carbohydrate-containing food on blood-glucose levels is called the glycemic response. The glycemic responses of various foods have been measured and then ranked in comparison to a reference food, usually a slice of white bread or just straight glucose, to create a numeric value called the glycemic index GI.
Foods that have a low GI do not raise blood-glucose levels neither as much nor as fast as foods that have a higher GI. However, GIP is only one of many potential GI hormones which could be candidates with a trophic activation of salivary gland amylase secretion. Clearly much more work is required to confirm or refute this explanation for our data. These additional studies could include the measurement of potential incretins and insulin in serial plasma samples from high- and low- salivary amylase secretors after ingesting a standard starch meal.
A potential rationale for why the glycaemic response of high salivary amylase secretors is less than that of low salivary amylase secretors. It is tempting to hypothesise that a prompt output of GIP might also serve to be a long-term stimulator of amylase secretion. Indeed, there is evidence that GIP stimulates the release of pancreatic amylase [ 21 ].
So it is feasible that GIP may also trophically stimulate the production and secretion of salivary amylase. If this were so, the habitual consumption of diets which are high in starch would result in a large release of GIP, which would in turn further stimulate salivary amylase production. Consumers of high-starch diets from such genetically or environmentally adapted groups would be anticipated to be substantially protected from glycaemia from early release of saccharides.
The resulting enhanced GIP secretion would induce insulin secretion, as a rapid and effective gastrointestinal anticipatory response, as found for the HA group in our present study. It is interesting to note that the evidence for the association between salivary amylase activity and obesity is currently inconclusive.
While there is data to suggest that low copy number of AMY1 was correlated with obesity [ 22 — 24 ], there is also evidence to the contrary [ 25 ].
As obesity is well-known to be associated with impaired glucose tolerance, the former finding is consistent with the data which we have reported in the present paper.
In short, previous reports suggest that the glucose tolerance of individuals secreting a low activity of salivary amylase is likely to be impaired when compared to the glucose tolerance of individuals who are high amylase secretors. Whether the difference in BMI between the high- and low-salivary amylase producers seen in our study may have contributed to our results is not certain, because of the small size of our experimental groups.
Never-the-less this data have to be interpreted with caution, because one of the inclusion criteria for our subjects in the first part of this study was to have a BMI between 18 and Moreover, the lack of a significant difference between the LA and HA subjects in their glycaemic responses to maltose and glucose, suggests that the difference seen with starch is not related to BMI, as otherwise we would have expected to observe it after administering boluses of all three carbohydrates.
Hence the effect may not have been as pronounced as the use of paraffin film to stimulate secretion. However, owing to cultural acceptance, this method was not used in the current study. We acknowledge that this could have affected the assessment of salivary amylase activities.
The differences between stimulated and unstimulated amylase activities require further investigation, as an additional contributor to variations in glycaemic response to a starch bolus. In brief, our results confirm in Asians earlier studies in American and Chilean Europeans, and show that, after a starch bolus, glycaemia from starch is lesser in high salivary amylase secretors, and greater in low salivary amylase secretors.
This explanation can account for the anomalies in our results for the glycaemic response to the digestion of starch, but, requires further studies to be refuted or validated. However, whatever the mechanism that underlies the seemingly anomalous results of our study, it is concluded that low amylase secretion may be a prognosticator for impaired glucose tolerance to dietary starch in young Malaysian adults.
This interesting concept paves the way for development and evaluation of a simple test of low salivary amylase, as a predictor of future or present impaired glycaemic tolerance to starch. Glycaemic responses to glucose and rice in people of Chinese and European ethnicity. Diabet Med. Read NW, et al. Swallowing food without chewing; a simple way to reduce postprandial glycaemia. Br J Nutr. Mandel AL, Breslin P. High endogenous salivary amylase activity is associated with improved glycemic homeostasis following starch ingestion in adults.
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