How long will diabetes stay away after weight loss? Long-term normal blood glucose control in previously diabetic individuals after bariatric surgery demonstrates that diabetes does not recur for up to 10 years, unless substantial weight gain occurs (86). These observations are consistent with the twin cycle hypothesis and the existence of a trigger level for adverse metabolic effects of fat in the pancreas. Hence, for a given individual with type 2 diabetes, reducing the liver and pancreas fat content below his or her personal trigger levels would be expected to result in a release from the fatty acid–mediated dysfunction. Individual tolerance of different degrees of fat exposure vary, and understanding this liposusceptibility will underpin the future understanding of genetically determined risk in any given environment. However, this should not obscure the central point: If a person has type 2 diabetes, there is more fat in the liver and pancreas than he or she can cope with.
In the study, Fung and his team randomly recruited three men, ages 40 to 67, with type 2 diabetes, who also had high cholesterol and high blood pressure. At the start of the study, the authors recorded the participants’ vitals, including their A1C (a three-month average of their blood sugar levels), their fasting blood glucose levels, their waist circumference, and their weight. All three men were on insulin and oral medication.
Diabetic patients must get professional dental cleanings every six months. In cases when dental surgery is needed, it is necessary to take some special precautions such as adjusting diabetes medication or taking antibiotics to prevent infection. Looking for early signs of gum disease (redness, swelling, bleeding gums) and informing the dentist about them is also helpful in preventing further complications. Quitting smoking is recommended to avoid serious diabetes complications and oral diseases.
Exenatide (Byetta) was the first drug of the GLP-1 agonist group. It originated from an interesting source, the saliva of the Gila monster. Scientists observed that this small lizard could go a long time without eating. They discovered a substance in its saliva that slowed stomach emptying, thus making the lizard feel fuller for a longer time. This substance resembled the hormone GLP-1.
The information on this website is provided as general health guidelines and may not be applicable to your particular health condition. Your individual health status and any required medical treatments can only be properly addressed by a professional healthcare provider of your choice. Remember: There is no adequate substitution for a personal consultation with your physician. Neither Desert Springs Hospital Medical Center, or any of their affiliates, nor any contributors shall have any liability for the content or any errors or omissions in the information provided by this website.
Some medical professionals use an Oral Glucose Tolerance Test (OGTT) to test for diabetes. If you’ve ever been pregnant and had to drink the sickeningly sweet sugar cocktail and then have blood drawn, you are familiar with this one. Basically, a patient is given 50-75 grams of glucose in concentrated solution and his blood sugar response is measured. I’m not a fan of this test because no one should be ingesting that much concentrated glucose, and the test is not a completely accurate measure. (Just a side note: if you are a drinker of the “Big Gulp” drinks or large amounts of soda, you are putting your body through a similar test each day! Eventually, your body will respond, probably with something like “Fine, you want diabetes, I’ll show you diabetes!)
Does acupuncture for diabetes work? Acupuncture has many uses, and some research has suggested that it may work for diabetes, although how it would help has not yet been explained. Find out about the types of acupuncture that might help, the risks, and some evidence of its benefits. Anyone considering acupuncture should first check with their doctor. Read now
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).
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.
Some people with diabetes use a computerized pump -- called an insulin pump -- that gives insulin on a set basis. You and your doctor program the pump to deliver a certain amount of insulin throughout the day (the basal dose). Plus, you program the pump to deliver a certain amount of insulin based on your blood sugar level before you eat (bolus dose).
Watch for thirst or a very dry mouth, frequent urination, vomiting, shortness of breath, fatigue and fruity-smelling breath. You can check your urine for excess ketones with an over-the-counter ketones test kit. If you have excess ketones in your urine, consult your doctor right away or seek emergency care. This condition is more common in people with type 1 diabetes but can sometimes occur in people with type 2 diabetes.
Exercise– Even the mainstream medical community recognizes the advantage of exercise, as it increases the muscles ability to use insulin and over time can help fix insulin resistance. All exercise isn’t created equal though and fortunately, smaller amounts of high intensity exercise have been shown to have a better effect on insulin levels (and weight loss) than an hour of daily moderate cardio. According to the Healthy Skeptic: “A pair of studies done at McMaster University found that “6-minutes of pure, hard exercise once a week could be just as effective as an hour of daily moderate activity“, according to the June 6, 2005 CNN article reporting on the study.” I recommend high intensity exercise anyway for its various health advantages, and it is great for diabetes control. too.
So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, but only for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.
Optimal management of diabetes involves patients measuring and recording their own blood glucose levels. By keeping a diary of their own blood glucose measurements and noting the effect of food and exercise, patients can modify their lifestyle to better control their diabetes. For patients on insulin, patient involvement is important in achieving effective dosing and timing.
Peripheral neuropathy is a problem with the functioning of the nerves outside of the spinal cord. Symptoms may include numbness, weakness, burning pain (especially at night), and loss of reflexes. Possible causes may include carpel tunnel syndrome, shingles, vitamin or nutritional deficiencies, and illnesses like diabetes, syphilis, AIDS, and kidney failure. Peripheral neuropathy is diagnosed with exams and tests. Treatment for the condition depends on the cause. Usually, the prognosis for peripheral neuropathy is good if the cause can be successfully treated or prevented.
Fix your Gut– Not the beer gut, your intestines. Grains and toxins cause damage to the intestinal lining and facilitate leaky gut syndrome. Depleted beneficial bacteria in the gut caused by poor diet, antibiotic use or being bottle fed as a baby can make the problem worse. Remove the grains, avoid toxins whenever possible and take a high quality probiotic to help the intestines heal. As a note: some people will have continued damage to the gut with exposure to grains, especially gluten, as little as only every 10 days or even every 6 months.
The primary issue requiring management is that of the glucose cycle. In this, glucose in the bloodstream is made available to cells in the body; a process dependent upon the twin cycles of glucose entering the bloodstream, and insulin allowing appropriate uptake into the body cells. Both aspects can require management. Another issue that ties along with the glucose cycle is getting a balanced amount of the glucose to the major organs so they are not affected negatively.
A history of blood sugar level results is especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Chinese medicine teaches us that we do not treat a patient based solely on a Western medical diagnosis, but, rather, based on the symptoms that present, and the health of the body as a whole system. There are several beneficial herbal formulas that have been developed to treat some of the general symptoms, but it is important to remember that not everyone will present symptoms in the same way, and treatment should be individualized to suit the specific needs of the patient.
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
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.