I made a mistake in an earlier comment that I need to correct. I thought the VLDL represented the very small particles, and that is totally wrong. Here are the actual test results of the very small particles from a Quest Diagnostics after about 18 months on a ketogenic diet, with abundant use of MCT oil as caprylic acid. If the administrator deletes that comment, to avoid confusion, that would be fine with me. I can also provide much more data, as that test is pretty comprehensive.

The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).

Alcohol: Alcohol can dangerously increase blood sugar and lead to liver toxicity. Research published in Annals of Internal Medicine found that there was a 43 percent increased incidence of diabetes associated with heavy consumption of alcohol, which is defined as three or more drinks per day. (8) Beer and sweet liquors are especially high in carbohydrates and should be avoided.
By checking your own blood sugar levels, you can track your body's changing needs for insulin and work with your doctor to figure out the best insulin dosage. People with diabetes check their blood sugar up to several times a day with an instrument called a glucometer. The glucometer measures glucose levels in a sample of your blood dabbed on a strip of treated paper. Also, there are now devices, called continuous glucose monitoring systems (CGMS), that can be attached to your body to measure your blood sugars every few minutes for up to a week at a time. But these machines check glucose levels from skin rather than blood, and they are less accurate than a traditional glucometer.
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCĪµ and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCĪ¶ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
Momordica Charantia goes under a variety of names and is native to some areas of Asia, India, Africa and South America. Marketed as charantia, it is also known as karela or karolla and bitter melon. The herb may be prepared in a variety of different ways, and may be able to help diabetics with insulin secretion, glucose oxidation and other processes.
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.