The more intense the exercise, the better. According to the British diabetes association diabetes.co.uk, high-intensity interval training (HIIT) may be better for weight loss and glucose control than continuous aerobic activity like jogging. HIIT involves alternating between short bursts of increased intensity exercise and rest — for instance, running and then walking on and off throughout the workout.
Type 2 diabetes mellitus is a condition in which the body cells develop resistance to insulin and fail to use it properly. Type 2 diabetes mellitus is more common amongst overweight and obese adults over 40 years of age. The disorder can also be referred to as non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes mellitus. Mostly, these patients need to manage their blood sugar levels through regular exercise, weight control, balanced diet, and anti-diabetes medications.
While Type 1 Diabetes is an autoimmune disorder that seems to affect people with certain gene types, Type 2 Diabetes is triggered by lifestyle choices, such as poor diet and obesity. Eating sugary and processed foods contributes to weight gain, and that extra body fat can be released into the bloodstream, impeding the absorption of insulin and other chemicals related to metabolism. When metabolism is slowed, weight gain is more likely, and the cycle repeats itself. Treatment for Type 2 Diabetes is multifaceted, often including insulin injections, a host of medications, and lifestyle modifications such as diet changes and exercise regimens.
Called ALA for short, this vitamin-like substance neutralizes many types of free radicals. A build-up of free radicals, caused in part by high blood sugar, can lead to nerve damage and other problems. ALA may also help muscle cells take up blood sugar. In a German study, a team of scientists had 40 adults take either an ALA supplement or a placebo. At the end of the four-week study, the ALA group had improved their insulin sensitivity 27 percent. The placebo group showed no improvement. Other studies have shown a decrease in nerve pain, numbness, and burning.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Dr. King said that even short-term remission would reduce or put off some of the serious complications associated with diabetes, like nerve damage, kidney damage, loss of vision, heart attacks and strokes. Yet structured weight loss programs are expensive and often not covered by insurance, and physicians — who are often not well-versed in nutrition — may not take the time to counsel patients about diet, Dr. King said.
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).
There is no prescribed diet plan for diabetes and no single “diabetes diet”. Eating plans are tailored to fit each individual's needs, schedules, and eating habits. Each diabetes diet plan must be balanced with the intake of insulin and other diabetes medications. In general, the principles of a healthy diabetes diet are the same for everyone. Consumption of various foods in a healthy diet includes whole grains, fruits, non-fat dairy products, beans, lean meats, vegetarian substitutes, poultry, or fish.