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).
The body’s immune system is responsible for fighting off foreign invaders, like harmful viruses and bacteria. In people with type 1 diabetes, the immune system mistakes the body’s own healthy cells for foreign invaders. The immune system attacks and destroys the insulin-producing beta cells in the pancreas. After these beta cells are destroyed, the body is unable to produce insulin.
Health2Sync helps you log your blood sugar, blood pressure, weight, medication, diet, exercise, and even your mood through the app. Health2Sync provides you helpful feedback based on your blood sugar records to help you manage diabetes. View current and past trends in your health. The app provides a diabetes support community. Invite your friends and family members to join you on your journey. Premium Features of the app include a PDF report feature.
Diabetic nephropathy (kidney damage). This is damage to the blood vessels in your kidneys. This means your kidneys have trouble filtering out waste. Some people who have nephropathy will eventually need dialysis (a machine treatment that eliminates waste from the blood) or a kidney transplant. The risk for nephropathy is increased if you have both diabetes and high blood pressure, so it is important to control both of these conditions. Protein in the urine is usually the first sign of nephropathy. This should be checked yearly.
According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.
Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk. The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk. Eating a lot of white rice appears to play a role in increasing risk. A lack of exercise is believed to cause 7% of cases. Persistent organic pollutants may play a role.
Effective therapy can prevent or delay diabetic complications.1,2 However, about 28 percent of Americans with DM are undiagnosed, and another 86 million American adults have blood glucose levels that greatly increase their risk of developing type 2 DM in the next several years.3 Diabetes complications tend to be more common and more severe among people whose diabetes is poorly controlled, which makes DM an immense and complex public health challenge. Preventive care practices are essential to better health outcomes for people with diabetes.4
You may be able to manage your type 2 diabetes with healthy eating and being active, or your doctor may prescribe insulin, other injectable medications, or oral diabetes medicines to help control your blood sugar and avoid complications. You’ll still need to eat healthy and be active if you take insulin or other medicines. It’s also important to keep your blood pressure and cholesterol under control and get necessary screening tests.
A1C blood test. This test provides information about a person’s average levels of blood glucose over the previous 3 months. The results are reported as a percentage. A normal A1C level is below 5.7 percent. If your A1C is higher than that, it means your blood sugar has been higher than normal. A test result of 6.5 percent or above indicates diabetes. A result between 5.7 and 6.4 indicates prediabetes.
The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).
^ Jump up to: a b c d Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, et al. (GBD 2015 Disease and Injury Incidence and Prevalence Collaborators) (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
Anna Syreeni, Niina Sandholm, Jingjing Cao, Iiro Toppila, David M. Maahs, Marian J. Rewers, Janet K. Snell-Bergeon, Tina Costacou, Trevor J. Orchard, M. Luiza Caramori, Michael Mauer, Barbara E.K. Klein, Ronald Klein, Erkka Valo, Maija Parkkonen, Carol Forsblom, Valma Harjutsalo, Andrew D. Paterson, for the DCCT/EDIC Research Group and Per-Henrik Groop, on behalf of the FinnDiane Study Group
Diabetes is a number of diseases that involve problems with the hormone insulin. Normally, the pancreas (an organ behind the stomach) releases insulin to help your body store and use the sugar and fat from the food you eat. Diabetes can occur when the pancreas produces very little or no insulin, or when the body does not respond appropriately to insulin. As yet, there is no cure. People with diabetes need to manage their disease to stay healthy.