An unbalanced microbiome composition, known as dysbiosis, has been found in patients with diabetes, for whom the diversity of the gut microbiome is often reduced as compared to healthy people. Researchers from the University of Amsterdam recently showed that fecal transplants, used to transfer the microbiome of a healthy person to the gut of one with diabetes, can result in a short-term improvement of the insulin resistance found in obese patients with type 2 diabetes.
These dietary recommendations have made high carb, low-fat foods a staple of the American diet. “Healthy” foods like fruit-on-the-bottom yogurt, sugary protein shakes and low-fat processed grains flooded the market. The standard American diet began to include more sugary drinks and sodas, as well as more processed grains. Since all carbohydrates (even complex carbs) are broken down into sugar in the body, these dietary recommendations meant that the average blood sugar of Americans began to rise – and the diabetes epidemic began to grow.
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).
A further danger of insulin treatment is that while diabetic microangiopathy is usually explained as the result of hyperglycemia, studies in rats indicate that the higher than normal level of insulin diabetics inject to control their hyperglycemia may itself promote small blood vessel disease. While there is no clear evidence that controlling hyperglycemia reduces diabetic macrovascular and cardiovascular disease, there are indications that intensive efforts to normalize blood glucose levels may worsen cardiovascular and cause diabetic mortality.
If the T2DM has been recently diagnosed, there is a greater likelihood of being able to reverse the disease. Doing this requires losing approximately 5-10% of current body weight, balancing carbs and protein and engaging in daily physical exercise. A diabetes educator (C.D.E.) is the expert who can help put together a plan for realistic and permanent lifestyle changes.
Focus on low glycemic index foods: While reducing fat and increasing fiber can significantly improve insulin sensitivity, low glycemic index (GI) foods reduce after-meal blood glucose levels. Low GI foods include pumpernickel or rye bread, oats, beans, bran cereals, most fruit, and sweet potatoes, compared to higher GI foods such as white potatoes, processed foods, and cold cereals.
The new research ties in with recent thinking among experts about what happens when type 2 diabetes develops, says Domenico Accili, MD, chief of endocrinology at Columbia University Vagelos College of Physicians and Surgeons. "We have been talking for some time, that in diabetes, primarily type 2, the insulin-producing [beta] cell is not dead but simply inactive," he says. "If you put patients with diabetes on a diet, you can do marvels with their beta cells."
If however, type 2 diabetes is a result of insulin resistance and being overweight, there is excellent evidence that exercise, decreasing added sugars and saturated fats in the diet, choosing low glycaemic index foods and losing weight – particularly around the abdominal region, can improve blood glucose levels to the extent that it seems like diabetes has been reversed.
Your care team may recommend that you use a continuous glucose monitor (CGM). A CGM is a wearable device that can measure blood sugar every few minutes around the clock. It's measured by a thread-like sensor inserted under the skin and secured in place. The more frequent CGM blood sugar readings can help you and the care team do an even better job of troubleshooting and adjusting your insulin doses and diabetes management plan to improve blood sugar control.
Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars better, but not the diabetes. We can pretend the disease is better, but that doesn’t make it true.
Most of us ignored the manual, just plugged it in and tried to figure out the rest. That’s why we all had the blinking 12:00 on. Today, most new electronics now come with a quick start guide which has the most basic 4 or 5 steps to get your machine working and then anything else you needed, you could reference the detailed instruction manual. Instruction manuals are just so much more useful this way.
If your carb consumption is on the high side (once you add sugar into the mix, you’re most certainly on the high side), it’s stored as fat and you end up with insulin resistance or non-alcoholic fatty liver disease. The reason behind it is that carbs metabolize into glucose, and limiting carbs helps your body control blood sugar more efficiently. It improves overall blood sugar profiles, insulin sensitivity, and hemoglobin A1c, which is a diabetes marker. Going low-carb is especially effective if you’re in the early stages when you do not yet need to administer insulin.
Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas. This release of insulin promotes the uptake of glucose into body cells. In patients with diabetes, the absence of insufficient production of or lack of response to insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.