Normally, serum glucose (blood sugar) will be 70 - 130 mg/dL (milligrams per deciliter)
[righthealth.com, downloaded 6 Oct 2009]. Although these numbers may [will] vary from person to
person, we can use these ‘typical’ values to understand how serum glucose regulation works.
When serum glucose in the hepatic portal vessel exceeds ‘normal,’ or 130 mg/dL, the excess
glucose is withdrawn from the serum at the liver, and a portion of the withdrawn glucose is converted
to glycogen for storage in the liver. Both the absorption of glucose and its conversion to glycogen
is mediated by insulin. Conversely, when serum glucose drops below ‘normal,’ or 70 mg/dL,
liver stored glycogen is converted to glucose [mediated by glucagon] and the glucose is dumped back
into the serum. These two processes generally keep the serum glucose in the hepatic vein within the
‘normal range.’ Similarly, in the circulating serum, all tissues can withdraw glucose as
needed again with insulin facilitating the absorption of the glucose into the cells. The muscle
tissue also utilizes insulin mediated conversion of glucose to glycogen for storage in muscle tissue.
Serum glucose should not go over 180 mg/dL immediately after eating [righthealth.com downloaded 6 Oct 2009]. An exception to the withdrawl of excess glucose by the liver occurs any time the serum glucose spikes above 180 mg/dL in the hepatic portal vessel. For our caveman ancestors, this would have happened very rarely, but with added processed sugars in foods, these spikes may occur often. These spikes overwhelm the liver's capacity to absorb glucose, and the glucose spike travels up the hepatic vein, then to the entire body. Minor spikes (probably in the 131 - 180 mg/dL range are possible causes of the ‘sugar high’ characterized by a feeling of euphoria attributable to the excess sugar available, but major spikes above 180 mg/dL are more likely to cause the ‘sugar crash’ characterized by a feeling of lethargy, attributable to the sugar “overdose.” The lethargy seems to persist until glucose drops back into the normal range, without a brief euphoria as it passes through the high 180 to 130 mg/dL range.
In the diabetic population, glucose metabolism is compromised, so glucose absorption by all tissues (liver, muscle, and other tissues) is impaired. As a result glucose spikes will persist longer than normal, and the patient will experience hyperglycemia. The release of glucose from the liver to the hepatic vein is also impaired, with episodes of hypoglycemia between the hyperglycemic episodes. As currently understood, diabetes comes in three forms: Type I, Type II, and Gestational diabetes. Each of these has to be managed, and the management regimes are different depending on which form of diabetes the patient has.
Type I diabetes was called ‘juvenile onset diabetes’ and was thought to be a genetic
disorder. It is now believed that the genetic basis of Type I diabetes involves a
‘pre-disposition’ to develop the disorder, not the cause of the disorder. Those individuals
who are pre-disposed to develop Tye I diabetes, there seems to be an environmental trigger
(tenatively identified as a viral infection, or allergic reaction to some [unidentified] allergan)
that causes an auto-immune attack which damages the pancreatic tissue responsible for insulin
production. The affected individuals are insulin deficient due to inadequate insulin production, and
are therefore ‘insulin dependant.’
“The main goal [in] the management of type I diabetes is blood glucose control” (Brown, 2008. Nutrition Now, Thompson Wadsworth). This requires regular, healthly meals at planned times plus planned physical activity. The food intake and exercise plans must consider the insulin dosing plan. The patient must monitor blood glucose several times a day, and must adjust their insulin dose accordingly.
Those patients most likely to develop Type II diabetes are over-weight (or sufficiently over-weight
to be obese), and inactive. About 90% of diagnosed Type II diabetics are over-weight, and 60% are
also diagnosed obese. There may be multiple genetic traits that predispose to developing Type II
diabetes, but as I understand genetics, no individual can “acquire very early in life …
multiple genetic traits” (Brown, 2008), nor even acquire a single genetic trait. At least
some patients seem to progress through several early stages which could be used as diagnostic
testing ultimately to prevent the disorder. The patient will exhibit chronic elevated fasting serum
glucose levels below the minimum considered to be diabetic, a condition called
prediabetes. Most patients currently diagnosed with prediabetes also
exhibit insulin resistance, a condition in which the insulin receptors on
cell membranes ‘resist’ [mechanism unknown] the effects of insulin as a facilitator of
glucose absorption by the cell. The wording of descriptions
(such as National Diabetes Information Clearing
House of the National Institutes of Health)
suggest that an underlying hypothesis is that insulin resistance may lead to prediabetes, and that
the precondition for insulin resistance is metabolic syndrome, which
“is defined as the presence of any three of the following conditions:
• waist measurement of 40 inches or more for men and 35 inches or more for women
• triglyceride levels of 150 milligrams per deciliter (mg/dL) or above, or taking medication for elevated triglyceride levels
• HDL, or “good,” cholesterol level below 40 mg/dL for men and below 50 mg/dL for women, or taking medication for low HDL levels
• blood pressure levels of 130/85 or above, or taking medication for elevated blood pressure levels
• fasting blood glucose levels of 100 mg/dL or above, or taking medication for elevated blood glucose levels”
(http://diabetes.niddk.nih.gov/DM/pubs/insulinresistance/, downloaded 6 Oct 2009).
So it is possible that metabolic syndrome may lead to insulin resistance
Insulin resistance may lead to prediabetes
Prediabetes may lead to Type II diabetes;
and if so, it may be possible to prevent (or reduce the incidence of) Type II diabetes by detecting any of the precursor conditions and starting an aggressive intervention to prevent (or at least reduce the risks for) the next stage of the progression. AND the best preventative measures should be to reduce the incidence of metabolic syndrome by making healthier lifestyle choices.
The management of Type II diabetes reads a lot like the advice for the healthier life style choices which would reduce the risks of developing metabolic syndrome.
There is a recent article in the journal Cell [Da Young Oh, et al, 2010. GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects Cell, Volume 142, Issue 5, 687-698, 3 September 2010] which describes a possible role of Ω-3 fatty acids in reducing the symptoms of Type-II Diabetes. The authors worked with mice (Wild Type, or WT, and GPR120 knockdown [a genetic modification in which the mice lack the cell receptor sites GPR120]. They demonstrated that the Ω-3 fatty acids bind to the receptor sites, preventing the “chronic macrophage-mediated tissue inflammation [which] is a key mechanism for insulin resistance in obesity … The ω-3 FA treatment [supplements comparable to the over-the-counter Ω-3 oil capsules] inhibited inflammation and enhanced systemic insulin sensitivity in WT mice, but was without effect in GPR120 knockout mice.” While the authors did not recommend Ω-3 fatty acid supplementation for the human population [because they have not yet begun the clinical testing on human subjects], this does suggest that an increase in Ω-3 fatty acids from food sources (white fish) may be worth trying as a way to reduce the symptoms of Type-II diabetes.
Two factors separate gestational diabetes from Type II diabetes. The onset of the disorder occurs during pregnancy, and it frequently disappears after delivery. However, patients who have been diagnosed with gestational diabetes seem to have a higher risk for developing Type II diabetes than the general population. A major issue in managing gestational diabetes is to manage the risks of developing Type II diabetes.
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