Diabetes and Diet Theraphy

Amaliah Harumi

Effect of Meal Frequency on BloodGlucose,Insulin,and FreeFattyAcidsinNIDDM Subjects

Diabetes Treatment, Part 1: Diet and Exercise Michael J. Fowler, MD

Substantial dietary restriction to 1,100 kcal/day has been shown to decrease fasting blood glucose of obese patients with diabetes and even in those without diabetes in as few as 4 days. This improvement was likely the result of decreased hepatic glucose output After 28 days of calorie restriction, there was further decline in the fasting glucose levels of obese diabetic subjects, and insulin sensitivity was significantly improved.

 It is also noteworthy that improvement in insulin sensitivity correlated well with decrease in fasting glucose and insulin sensitivity. These results occurred with an average weight loss of only 6 kg. These studies did not show an improvement in insulin secre-tory capacity.

Carbohydrate
Carbohydrate and monounsaturated fat should comprise 6070% of total calories. However, there is some concern that increased unsaturated fat consumption may pro-mote weight gain in obese patients with type 2 diabetes and thereby decrease insulin sensitivity.

Protein
Patients with type 2 diabetes exhibit a more negative nitrogen balance than individuals without diabetes. Protein degradation appears to be exacerbated by hyperglycemia and improved by controlling glucose levels with insulin therapy

 Studies of patients with type 2 dia-betes, however, have demonstrated that protein consumption does not increase plasma glucose concentrations and that endogenous insulin release is, in fact, stimulated by protein consumption There may also be an association between high-protein diets and the risk of developing diabetic nephropathy

An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes

when protein was given with glucose, a synergistic effect on insulin was observed. As a result, the glucose area response was significantly less after ingestion of protein plus glucose than after ingestion of glucose alone.

GLUT2 mutations, translocation, and receptor function in diet sugar managing

Glucose homeostasis depends on the ability of the various tissues to detect and signal sugar abundance or scarcity to build or mobilize sugar stores. In addition to such acute regulations, tissues are able to adapt in the long term to the amount of dietary sugar. Interestingly, the intestine, pancreas, kidney, and liver, which all play key roles in the handling of dietary sugars, express the glucose/ fructose transporter GLUT2

 Briefly, refeeding after a fast or low- vs. highcarbohydrate diets modulate GLUT2expression in the intestine, kidney, liver, and pancreas Low insulin and high glucose levels in streptozotocin-induced diabetic rodents increase GLUT2expression in the intestine and liver (47, 84), suggest-ing that glycemia and insulinemia control GLUT2expression

 Conversely, remarkable reductions inGLUT2expression have been found in the diabetic pancreas (74), and in the liver and intestine in an animal model of parenteral nutrition (8), show-ing that other factors, in addition to glucose or insulin, regulate GLUT2 expression.

 Use of dietary fibre of the guar type in mild diabetics may be associated with an appreciable reduction of post parandial glycosuria and allows an increased carbohydrate intake. It may also protect susceptible individuals from insulin induced hypoglycemia by facilitating slower absorbtion of glucose. this would allow the blood glucose to be maintained therapeutically at more nearly "normal" levels. Findings have also suggested prolongation of mouth to caecum transit time by this storage polysaccharide.

 Co-ingestion of glucose and fibre blunts the glycemic response. This isapparently related to delayed gastric emptying and slower rate of glucose absorption. There is also limited evidence that some component

 When eating a meal rich in carbohydrate, insulin levels rise and glucagon levels fall. The decrease of glucagon is due to inhibition of its release by insulin, and to the elevation in plasma glucose

 When eating a meal rich in protein, insulin levels rise, because insulin secretion is stimulated by amino acids. Glucagon levels also rise; glucagon release is also stimulated by amino acids. In this case, unopposed insulin action would result in hypoglycemia, since little glucose is being absorbed; glucagon must increase to maintain plasma glucose

 When eating a mixed meal, insulin levels rise, and glucagon levels rise, fall, or remain unchanged as appropriate to maintain plasma glucose. The pancreas uses its ability to monitor the influx of nutrients, supplemented by signals in the form of intestinal peptide hormones, to regulate the disposal of the nutrients without allowing an undue change in plasma glucose (glucose levels usually rise to the upper limit of the normal range, ~120 mg/dL, but little further). Mimicking this tailored change in pancreatic hormone release is difficult to achieve by injections of insulin, and explains part of the problem faced by individuals with Type I diabetes.

Carbohydrates and Diabetes

he ADA specifically states that "low-carbohydrate diets (restricting total carbohydrate to < I 3 0 g/day) are nor recommended in the management of diabetes" (ADA, 2006b

Komplikasi paling dkt

Glukosuria , diuresis, sel langerhans glut 4, insluin ningkatin glukosinase Sel yg ga butuh insulin jd nyimpen glukosa tp jd bikin produk yg aneh2 Dm awal insulin tinggi krn feedback positif lama2 cape sintesisnya turun.