diabetes and diet theraphy

7/30/2019 Diabetes and Diet Theraphy

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Diabetes and Diet Theraphy

Amaliah Harumi


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Effect of Meal Frequency on

BloodGlucose,Insulin,and

FreeFattyAcidsinNIDDM

Subjects


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Diabetes Treatment, Part 1: Diet and Exercise

Michael J. Fowler, MD

Substantial dietary restriction to 1,100 kcal/dayhas been shown to decrease fasting bloodglucose of obese patients with diabetes and even

in those without diabetes in as few as 4 days.This improvement was likely the result ofdecreased hepatic glucose output

After 28 days of calorie restriction, there was

further decline in the fasting glucose levels ofobese diabetic subjects, and insulin sensitivitywas significantly improved.


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It is also noteworthy that improvement in

insulin sensitivity correlated well with

decrease in fasting glucose and insulinsensitivity.

These results occurred with an average

weight loss of only 6 kg. These studies did notshow an improvement in insulin secre-tory

capacity.


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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.


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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


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Studies of patients with type 2 dia-betes,however, have demonstrated that proteinconsumption does not increase plasma

glucose concentrations and that endogenousinsulin release is, in fact, stimulated byprotein consumption

There may also be an association betweenhigh-protein diets and the risk of developingdiabetic nephropathy


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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 signifi-

cantly less after ingestion of protein plus

glucose than after ingestion of glucose alone.


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GLUT2 mutations, translocation, and receptor function in diet

sugar managing

Glucose homeostasis depends on the ability ofthe various tissues to detect and signal sugarabundance or scarcity to build or mobilize sugarstores.

In addition to such acute regulations, tissues areable to adapt in the long term to the amount ofdietary sugar.

Interestingly, the intestine, pancreas, kidney, and

liver, which all play key roles in the handling ofdietary sugars, express the glucose/ fructosetransporter GLUT2


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Briefly, refeeding after a fast or low- vs. high-

carbohydrate diets modulate

GLUT2expression in the intestine, kidney,

liver, and pancreas

Low insulin and high glucose levels in

streptozotocin-induced diabetic rodentsincrease GLUT2expression in the intestine and

liver (47, 84), suggest-ing that glycemia and

insulinemia control GLUT2expression


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Conversely, remarkable reductions

inGLUT2expression have been found in thediabetic 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.


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Use of dietary fibre of the guar type in mild diabeticsmay be associated with an appreciable reduction ofpost parandial glycosuria and allows an increasedcarbohydrate intake.

It may also protect susceptible individuals from insulininduced hypoglycemia by facilitating slowerabsorbtion of glucose. this would allow the bloodglucose to be maintained therapeutically at more

nearly "normal" levels. Findings have also suggested prolongation of mouth to

caecum transit time by this storage polysaccharide.


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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 limitedevidence that some component


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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


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When eating a meal rich in protein, insulinlevels rise, because insulin secretion isstimulated by amino acids.

Glucagon levels also rise; glucagon release isalso stimulated by amino acids. In this case,unopposed insulin action would result inhypoglycemia, since little glucose is beingabsorbed; glucagon must increase to maintainplasma glucose


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When eating a mixed meal, insulin levels rise, and glucagonlevels rise, fall, or remain unchanged as appropriate tomaintain plasma glucose.

The pancreas uses its ability to monitor the influx ofnutrients, supplemented by signals in the form of intestinalpeptide hormones, to regulate the disposal of the nutrientswithout allowing an undue change in plasma glucose(glucose levels usually rise to the upper limit of the normalrange, ~120 mg/dL, but little further).

Mimicking this tailored change in pancreatic hormonerelease is difficult to achieve by injections of insulin, andexplains part of the problem faced by individuals with TypeI diabetes.


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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


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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.

diabetes and diet theraphy

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