In medical world, diabetes is known more commonly by the name of diabetes mellitus. In simpler and day-to-day language, it is referred as diabetes. It is a group of metabolic diseases in which a person has high blood sugar, either because cells do not respond to the insulin that is produced, or the body does not produce enough insulin. In both the conditions, the body is not able to get enough amount of insulin to function properly.
Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
But does Darkes' story really mean type 1 diabetes can be cured? Darkes declined to provide his medical records, and the experts Live Science spoke to said there were several missing or confusing pieces of information in his story. Usually, incredible medical stories like this one are reported as case reports in the medical literature, the experts said. And even if the details of his story can ultimately be confirmed, the experts emphasized that it's extremely unlikely that Darkes' case would lead to a widespread cure for type 1 diabetes, as reports in the media have wrongly suggested.
Effect of an 8-week very-low-calorie diet in type 2 diabetes on arginine-induced maximal insulin secretion (A), first phase insulin response to a 2.8 mmol/L increase in plasma glucose (B), and pancreas triacylglycerol (TG) content (C). For comparison, data for a matched nondiabetic control group are shown as ○. Replotted with permission from Lim et al. (21).
You should have no more than three of these “feeding times” per day. The reason limiting the number and duration of your meal times is so important has to do with staying out of the vicious cycle of increasing insulin resistance. To get smart on insulin resistance — the cause of both type 2 diabetes and obesity — read Dr. Jason Fung’s book, The Obesity Code: Unlocking the Secrets of Weight Loss, or watch his free lecture on YouTube.
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