Type 2 diabetes mellitus is characterized differently and is due to insulin resistance or reduced insulin sensitivity, combined with relatively reduced insulin secretion which in some cases becomes absolute. When glucose levels become depleted, glucagon and cortisol levels rise significantly to enhance gluconeogenesis. Up-regulation (receptors) occurs with insulin after 4 weeks of exercise to increase its sensitivity (diabetic importance). This material is based upon work supported by the Nursing, Allied Health and Other Health-related Educational Grant Program, a grant program funded with proceeds of the State’s Tobacco Lawsuit Settlement and administered by the Texas Higher Education Coordinating Board.
I was both confounded and surprised because my diet is pretty darn excellent, particularly concerning those pesky, debilitating high glycemic carbs that proliferate the Great American Diet. If you haven’t read My Blood Sugar Numbers Confound Me, you may wish to do so before continuing so that you can have context for the rest of this post. The first thing that occurred to me when I got my blood test results was that both my father and uncle (his brother) developed adult-onset diabetes, which is called “Type 2 Diabetes”. I always thought that they both contracted that disease in their 60s because they ate crap, were overweight and didn’t exercise, but now I’m wondering if they had a genetic predisposition to type 2 diabetes and therefore would have gotten it even if they ate and exercised…ahh… well… like me? As the video in “My Blood Sugar Numbers” describes, I borrowed my sister’s glucometer and began testing my blood. In addition to the favorable post meal blood glucose numbers, I have another blood measurement marker that’s in my favor. Hemoglobin A1(c) is expressed in percentage terms because it’s measuring the percentage of hemoglobin that’s bonded to sugar.
In subsequent posts, I’ll report about some other unhappy blood result I got in my last Life Extension test, such has high VLDL, Pattern B LDL Density Pattern, high inflammation markers and low thyroid indications.


You're gonna get (1) the Newsletter, (2) the four-part guide, Transform Your Body and Mind, and (3) the 12 Ageproof Biohacks. HNF-4α controlling many genes involved in liver function such as the GLUT2 and L-PK genes.
Evidence on the mode of action of metformin shows that it improves insulin sensitivity by increasing insulin receptor tyrosine kinase activity and enhancing glycogen synthesis in hepatocytes, and by increasing recruitment and transport of GLUT4 transporters to the plasma membrane in adipose tissue. In addition to its effects on hepatic glucose and lipid homeostasis and adipose tissue lipid homeostasis, metformin exerts effects in the pancreas, vascular endothelial cells, and in cancer cells.
I’ve been testing fasting blood glucose, and one and two hour post meal, the detailed results of which I’ll share in a future post. This measures how much glucose permanently gets glycated (bonded) to hemoglobin in red blood cells. I'm a big believer in sustainability, and am a bit nutty about optimizing my diet, supplements, hormones and exercise.
Alcohol and snacking (assuming the snacks are high glycemic) will boost blood sugar and over time that could cause insulin resistance. Another exenatide-related drug is Bydureon® which is a once-a-week injectable form of exenatide.
A more recent addition to the GLP-1 receptor agonist family of diabetes drugs is Trulicity® (dulaglutide) manufactured by Eli Lilly and Co. Additionally, it has been shown that metformin affects mitochondrial activities dependent upon the model system studied. The latter effects of metformin were recognized in epidemiological studies of diabetic patients taking metformin versus those who were taking another anti-hyperglycemia drug.


This measurement roughly indicates your average blood sugar over the previous three months, and the higher it has been over the past three months, the more likely it is that glucose (sugar) is permanently bonded to hemoglobin, which is not a good thing. He reports that it’s not uncommon for people on restricted carbohydrate diets (like me) to have high fasting glucose serum numbers. If you legitimately are on a low-carb diet and both the post meal and A1(c) numbers are good, then it could be that your situation is accurately described by Chris’ explanation quoted above. Metformin has a mild inhibitory effect on complex I of oxidative phosphorylation, has antioxidant properties, and activates both glucose-6-phosphate dehydrogenase, G6PDH and AMP-activated protein kinase, AMPK. The importance of AMPK in the actions of metformin stems from the role of AMPK in the regulation of both lipid and carbohydrate metabolism (see AMPK: Master Metabolic Regulator for more details). In adipose tissue, metformin inhibits lipolysis while enhancing re-esterification of fatty acids. The activation of AMPK by metformin is likely related to the inhibitory effects of the drug on complex I of oxidative phosphorylation.
This would lead to a reduction in ATP production and, therefore, an increase in the level of AMP and as a result activation of AMPK. In fact, since the cells of the gut will see the highest doses of metformin they will experience the greatest level of inhibited complex I which may explain the gastrointestinal side effects (nausea, diarrhea, anorexia) of the drug that limit its utility in many patients.



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Comments

  1. 13.12.2013 at 12:16:27


    Blood within 15 minutes which is helpful for a diabetic experiencing patient's.

    Author: Lizok
  2. 13.12.2013 at 15:42:26


    HbA1c levels (and therefore, any improvement many.

    Author: Ilgar_10_DX_116