There’s a lot of contradictory information on the question of whether pancreatic beta cell dysfunction or Insulin Resistance is the cause of Type 2 Diabetes. Our previous post shows the Insulin Resistance leading (Type 2 Diabetes is not a Problem of Too Little Insulin).
This study shows the other side (Front Endocrinol (Lausanne). 2013; 4: 37. Beta Cell Dysfunction and Insulin Resistance. Marlon E. Cerf). The study has:
Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes. Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis.
It sounds like there’s a bit of a chicken-and-egg scenario going on. It is also established that higher blood sugar levels will cause beta cell damage. The study goes on to state:
Beta cell dysfunction is the critical determinant for type 2 diabetes (Ashcroft and Rorsman, 2012) which is compounded by insulin resistance.
The paper presents a Catch-22.
Glucose is therefore a critical determinant of beta cell function – persistent hyperglycemia may exhaust beta cells whereas hypostimulation may prime beta cells for low glycemic states (fasting and starvation) potentially limiting their response to hyperglycemic excursions.
So if you keep the blood sugar high then beta cells may be exhausted (burned-out). If you drop the stimulus then your ability to respond to a stimulus may also be reduced. The only solution is to not exhaust the beta cells in the present and not do future high glucose loads.
I think the question is one of timing. This all moves in phases which may vary for some people. As an example, unlike me, not all diabetics have rapid weight loss. The study presents some of this point:
Therefore adiposity, and particularly fat in the pancreas and major glucose recipient organs, will exacerbate insulin resistance which consequently impairs beta cell function. Obesity also increases insulin demand therefore hyperfunction of beta cells may exhaust beta cells resulting in beta cell dysfunction.
The study actually presented the other side.
Beta cell dysfunction signals an advanced state of diabetes as insufficient insulin is secreted to meet demand. Insulin resistance precedes the pathogenesis for several modern diseases (Samuel and Shulman, 2012). Thus understanding the pathogenesis of insulin resistance has become increasingly important to guide the development of future therapies and inform health and economic policy (Samuel and Shulman, 2012).
Another valid point:
There is also an inverse correlation between the amount of fat in the human pancreas and GSIS, with glucose tolerance and insulin secretion improving in parallel with a reduction in pancreatic fat (Tushuizen et al., 2007).
More on the tipping point.
Beta cells initially compensate for the insulin resistance associated with obesity by increasing insulin secretion (Kasuga, 2006). When beta cell loss reaches the point of causing hyperglycemia, the beta cell replication rate is presumably maximally stimulated; therefore a further elevation in glucose concentrations will not increase replication (Porat et al., 2011). Glucose homeostasis maintains normoglycemia by adapting the mass and function of beta cells that counter insulin resistance, reduced beta cell mass, and excess nutrition (Liu et al., 2001).
Fortunately beta cells can be repaired/replaced. That only happens in lower blood sugar levels. That’s best done with low carbohydrate diets.
Diet as a solution?
Patients with poorly controlled type 2 diabetes who were placed on a hypocaloric diet for up to 12 weeks experienced a marked and rapid decrease in liver fat content (85%), associated specifically with normalization in hepatic insulin sensitivity and reductions in fasting hyperglycemia and hepatic glucose production without changes in intramyocellular lipid or insulin-mediated whole body glucose disposal (Petersen et al., 2005).