Diabetes mellitus has two distinct but quite differet forms. Type 1 due to lack id insulin production and type 2 an excess of glucose that insulin production can no longer control. Insulin resistance is cited as an issue when the physiological issue is too much glucose. Until glucose consumption is targetted in the management of type 2 diabetes mellitus, the underlying cause will not be addressed, contributing to phararmacologic and surgical interventions when diet modifiction is what is needed
This is a fascinating question with many angles.
Glucose consumption, type of dietary carbs, daily calorie restriction/excess are some of the sub texts here.
On a wider angle: the atherosclerosis [ and even some microvascular complications] predate the diagnosis of Dysglycaemia- so is it primarily a vascular disease?
The lipids are just as dysfunctional: one can even do a "lipid tolerance test" to show this. Poor lipoprotein disposal after a meal leads to prolonged exposure of the vasculature to small, dense LDL in Diabetes, thereby accelerating atherosclerosis. So , could Diabetes be a Lipid disease?
it is one cause of DM2 but there are many other causes like incorrect insulin madding by beta cell
The decrease of glucose uptake by liver and muscle cells are the main cause of DM, due to cell insensitive to insulin or shortage of insulin quantity or insulin with impaired quality.
For type 2 diabetes, the culprit is the insulin resistance. High carbs intake is one of the risk factors.
Supporting this idea is the fact that, metabolic surgery may reverse most of the cardiovascular risk factors associated with type 2 diabetes including the glucose profile in patients with high body mass index. So in genetically predisposed people, glucose consumption may play a major role.
The short answer is NO.
Glucose is essential for brain function and even excess glucose (4x normal) does not cause diabetes in rats in at least 6 months. This has been our observation, the animals are of course more sturdy than humans and they seem to be resistant to high glucose effects.
Now, in general, high glucose should promote some damage to the beta-cells and to produce such damage it will take a long time because of presence of anti-oxidants, body defense etc.
As you know the reason for type 2 diabetes is either insulin resistance or lack of insulin. The high glucose seen in majority of cases of diabetes is an effect rather than a cause. But it certainly can contribute to the progression of diabetes.
Regards
a recently published randomized controlled trial indicated that, sucrose containing drinks are not harmful unless if they lead to weight gain, a more recent animal trial showed that the effects of the first line anti-diabetic medication metformin could be due to microbiota effects (a decrease in M.Fragilis) and thus modulation of bile acids genes.
A recent study shows that sweetened drinks increases type 2 diabetes risk.
Food sources of fructose-containing sugars and glycaemic control: systematic review and meta-analysis of controlled intervention studies
https://www.bmj.com/content/363/bmj.k4644
Type 2 diabetes: sweetened drinks pose greater risk than other sugary foods
https://www.bmj.com/content/363/bmj.k4943
I guess IT CAN, but still diabetes remain the disease of lifestyle, so NOT ALWAYS
I think it is one of the predisposing factor for Type II diabetes, but there are more factors related to the muscle and lipid cells physiology, like insulin receptors and compound GLUT 4 in these cells.
For Type 2, the inability of the hepatocytes receptors to dock insulin (Insulin insensitivity) to effect its downstream hypoglycemic processes is the core brain behind its occurrence. So, glucose have no option but to build itself up in the blood (Hyperglycemia). So, we could say the hyperglycemia is an effect of insulin insensitivity. However, in vitro cellular studies with different cell lines (Glomerular Mesangial Cell (SV40) and HK2) have shown that high glucose condition could induce diabetic condition. This implies that a prolong intake of excessive glucose could therefore provoke some metabolic disregulation or associated signaling pathways and proteins that the cellular immune system might not be strong enough to fight.
I think that increasing glucose levels ( which leads to wight gain) may indirectly causes DM II .
High glucose levels together with free fatty acids and insulin resistance may lead to beta cell damage (lipoglucotoxicity)
Both glucotoxicity and lipotoxicity are inversely proportionate with the pancreatic insulin production function
Insulin resistance or beta cell failure. Without any of these T2DM does not develop regarding excess glucose.
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