Insulin deprivation in type I diabetes has, somewhat simplistically, been likened to starvation. It’s no surprise, then, that a few weight obsessed type I diabetic teens got the idea to reduce or occasionally skip their insulin injections as a means of weight control.
According to a CNN report the practice is known as diabulimia and has, with the help of Internet message boards, become increasingly popular, tried by as many as one third of type I diabetic women in the U.S. The report highlights the addictive nature of the problem and the risk of microvascular complications when the behavior is sustained over time.
Unfortunately the piece falls short in explaining diabulimia’s effects on the body with statements such as: “When sugars are high, the kidneys work overtime to filter the excess glucose from the blood.” Not exactly. Just the opposite, if anything. The kidneys work overtime NOT to excrete glucose by revving up the process of proximal tubular reabsorption, the capacity of which is exceeded in hyperglycemia due to increased concentration of glucose in the glomerular filtrate. Hyperfiltration does in fact occur in early diabetic nephropathy, though lacking in any teliologic explanation that I am aware of and involving mechanisms incompletely understood.
Added to the risk of microvascular disease is the threat of ketoacidosis. If weight loss, especially rapid weight loss is one’s goal then ketosis, the “smoke” of burning fat, might be considered desirable. But the ketosis of uncontrolled type I diabetes differs in at least one important respect from that of fasting in the normal individual due to inability of a self-regulating feedback mechanism in type I diabetes as will be explained below.
Insulin’s anti-ketotic mechanism involves two molecular sites, the first of which is the adipocyte and the second of which is the mitochondrial membranes in the hepatocyte. Insulin’s action on the adipocyte is the inhibition of hormone sensitive lipase (HSL). In insulin lack (or, in stress, a reduction in the ratio of insulin to counter-regulatory hormones) HSL is activated, leading to breakdown of stored triglyceride to glycerol and free fatty acid (FFA). Insulin lack at the level of hepatocytes creates a “ketogenic mode” in the liver which allows the beta oxidation of FFA to ketone bodies. This occurs via activation of carnitine palmitoyltransferase-1 (CPT-1), an enzyme which mediates attachment of a carnitine molecule to the fatty acid thus enabling entry into the mitochondria for beta oxidation.
Non type 1 diabetics have endogenous insulin. Fasting in such individuals causes ketosis. However, ketone bodies and FFAs feed back on the pancreas causing it to secrete a small amount of insulin, enough to partially inhibit HSL, thus limiting the supply of FFA to the liver and preventing ketoacidosis. (Exceptions are lactation, late pregnancy and some instances of acute alcoholism, states in which this system of checks and balances is defective). In type 1 diabetics this feedback mechanism is unavailable due to an absolute, or nearly absolute, lack of endogenous insulin.
Via Kevin M.D. and Clinical Cases and Images.