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Information about the diabetes based on info i have


INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 24


A. Sundaram* , C. R. Anand Moses*, S. Ilango*, V. Seshiah**


The basic defects in Type 2 diabetes consist of (1)

Insulin deficiency (2) Insulin resistance and (3)

increased hepatic glucose production (HGP) leading

to glucotoxicity, beta cell exhaustion and finally

beta cell failure. The treatment strategies to

overcome these defects are:

1) Modified meal Plan

2) Exercise

3) Blood glucose lowering drugs and

4) Insulin

The current oral blood glucose lowering agents and

dietary measures only partially correct the multiple

metabolic defects in NIDDM with insulin resistance

remaining relatively impervious to treatment

Hypoglycaemia and secondary failure are common

with presently available sulphonylureas and hence

the need for newer blood glucose lowering drugs. In

case of NIDDM, a successful new drug should

correct atleast one of the major underlying

metabolic disturbances. i.e. reduce insulin

resistance, enhance insulin production and secretion

in response to glucose, suppress exessive hepatic

glucose production or improve glucose uptake and

utilisation in peripheral tissues particularly, skeletal

muscle. Within the last few years three new groups

of drugs have been identified and they are:

a) Alpha glucosidase inhibitors, eg. Acarbose

b) Insulin Sensitizer, eg. Troglitazone.

c) Insulin secretoguogues, eg. Glimepiride and


The following review will discuss each of these

groups of drugs in detail.


In human salivary amylase, pancreatic amylase and

alpha-glucosidase are the enzymes involved in the

digestion of starch. All complex carbohydrates like

starch and sucrose have to be converted to simple

carbohydrates in the small intestine by an enzyme

alpha-glucosidase before absorption. Drugs which

inhibit the action of alpha-glucosidase known as

glucosidase inhibitor, preventing the breakdown of

complex carbohydrates thereby delay or preventing

carbohydrate absorption. Glucosidase inhibitors are

three types:

1. Reversible competitive inhibitors of alphaglucosidase.

eg: a. Acarbose; b. Meglital

2. Irreversible glucosidase inhibitor eg:


3. Powerful Sucrose inhibitor eg: Veglibose.

Acarbose is freely available for clinical use. Other

drugs are under clinical trial.


Acarbose is a psuedotetrasaccharide and is a

reversible competitive inhibitor of the brush border

alpha glucosidases (mainly glucoamylase, sucrose

and maltose) as well as alpha amylase. Acarbose

binds to alpha-glucosidase with high affinity.

Mode of Action:

1. Acarbose blocks the digestion of starch, sucrose

and maltose. The digestion of carbohydrate is

delayed and occurs throughout the small

intestine, rather than upper part of jejunum.

Absorption of glucose and other

monosaccharides in not affected. The net result

is a decrease in post prandial rise in blood

glucose. Most of the carbohydrate is eventually

absorbed and that which is now absorbed is

metabolised by the bacteria in the colon to short

chain fatty acids which are then absorbed in the


2. Acarbose decreases meal stimulated secretion of

gastric inhibitory polypeptide and other

gastrointenstinal peptide (inhibitors) hormones.

There is smaller increase in post prandial blood

sugar level that leads to smaller increase in

insulin level.

3. Acarbose does not cause weight gain with the

therapeutic doses.

* Dr. Ambedkar Institute of Diabetes, Govt. Kilpauk Medical College & Hospital Chennai-600 010.

** Chief Diabetologist, Apollo Hospitals, Chennai-600 006.

INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 25

Side Effects:

Abdominal fullness, borborygmi, increased

intestinal flatulence and diarrhoea are major side

effects of alpha-glucosidase inhibitors. These side

effects are due to undigested sugars passing through

large bowel where bacterial fermentation occurs,

producing both carbondioxide and large quantities

of osmotically active glucose load, leading to

diarrhoea and flatulence. These symptoms occur in

the first few weeks of treatment and abate with

continued long term treatment.

Degradation of Acarbose :

Mostly occurs in the intestine. Some of the

degradation products and the trivial amount of the

parent drug enter systemic circulation and are

excreted in urine. When high doses of Acarbose is

used, liver enzymes level should be checked.

Concomitant use of antacids, bile acid resins,

intestinal absorbents, or digestive enzyme

preparations may interfere with the effectiveness of

acarbose and should be used with care.

Contraindications to Acarbose use are primary

therapy for Type 1 diabetes, significant

gastrointestinal disorders and pregnancy or


Acarbose is administered orally three times a day

and chewed with the first mouthful of food. Initial

dose is 50 mg. Three times a day. Two weeks later

the dose is increased to 100 mg, thrice daily and

thereafter at 4 weeks interval, the dose is increased

upto 200 mg. Thrice daily or until the required

glycaemic control is achieved.

Uses :

In non-diabetics and in Type 2 diabetics acarbose

produces a dose related decrease in post-prandial

hyperglycaemia. Acarbose theraphy causes a

corresponding reduction in post prandial plasma

insulin response. Long term treatment either as

monotheraphy or in combination with S.U, acarbose

improves basal blood sugar concentration as well.

Thus insulin resistance decreases and sensitivity

improves consequent to reduction in


1. Primary Therapy:

When FBS is less than 11.1 mmol, acarbose is

said to decrease FBS by 1 mmol,

PPBS by 3 mmol and HbA1c by 1% Acarbose

does not cause hypoglycaemia when used as

primary therapy.

2. As an adjuvant to:

Sulphonylurea, b. Metformin and c. Insulin in

Type 2 DM. A reduction in the dosage of these

drugs occur when Acarbose is used as an


3. Acarbose decrease serum TGL in patients with

hypertriglycidemia by decreasing VLDL


4. Acarbose in impaired glucose tolerance:

Acarbose has been tried in persons with IGT for

prevention and postponment of onset of Type 2


5. In IDDM:

Long term treatment with acarbose reduces both

post prandial and basal hyperglycaemia and

reduces insulin requirement by 10 to 30 %

interestingly, episodes of hypoglycaemia

between meals may be less frequent and less

severe in IDDM.

In treatment of hypoglycemia in patients taking

acarbose, only oral or IV (glucose) should be given.

Sucrose and other complex carbohydrates should

not be used.

For Further Reading:

1. Rebovitz H. Oral hypoglycemic agents. In: Joslin’s

Diabetes Mellitus. Eds. Kahn and Weititr GC, Lea and

Febiger, Philadelphia, 1994; 521-2.

2. Bailey CJ, Williams G, Pickup J. New drugs in the

management of diabetes and its complications. Text book

of diabetes, Eds Pickup J and williams G. Blackwell,

London 1997; 84.5 – 6.

3. Jean-Louis Chaisson et al. The efficacy of Acarbose in the

treatment of patients with NIDDM – Annals of Internal

medicien 1994’ 928-35.

4. Marlkolf Hanefeld et al. Therapeutic Potentials of

Acarbose as a first line drug in NIDDM subjects

insufficiently treated with diet alone. Diabetes Care. 1991;


5. Sat Hit Vanasaeng et al. Effects of Alpha-glucosidase

inhibitor(acarbose) combined with sulphonylurea or

Sulphonylurea and metfermin in treatment of NIDDM. J.

Med Asse, Thai 1995; 18: 578-84.

6. Caniff RF, Shapire JA et al, Reduction of Glycosylated

haemoglobin and post prandial hyperglycaemia by

Acarbose in patients with NIDDM. Diabetes Care, 1995;

18: 817-24.

INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 26


Insulin deficiency, insulin resistance and increased

hepatic glucose output are the hallmark of

pathogenesis of Type 2 diabetes. Sulphonylureas

increase insulin secretion and may improve insulin

sensitivity while the biguanide metformin improves

insulin action. One of the exciting areas in the

management of Type 2 diabetes is the development

of pathogentically targetted drugs to overcome

insulin resistance, namely the thiozolidinediones.

They work mainly by reducing peripheral insulin

resistance in adipocytes, skeletal muscles and to a

lesser extent by decreasing hepatic glucose

production. These drugs facilitate insulin action in

liver, muscles and adipose tissue. They do not

stimulate insulin secretion. Pioglitazone, englitazone

and troglitazone are the thiozolidine derivatives.

Only Troglitazone is in clinical use. Troglitazone

was developed in 1980 and was synthesized later

with an alpha-tocopheral substitution and has antioxidant

properties in addition to improving insulin


Mechanism of Action of Troglitazone:

In Adipose Tissue :

1. Thiozolidinediones increase glucose oxidation,

lipogenesis and increase the expression of

GLUT-4, the glucose transporters in adipose


2. Recently these drugs are found to interact or

bind with the PPAR-Y (Peroxidase Proliferator

Activated receptor –Y) nuclear receptor of

adipocytes. PPAR – Y is the binding site for

troglitazone and this leads to differentiation of

insulin resistant large size adipocytes, into

insulin sensitive small adipocytes, without

increasing adipocyte mass and thereby reducing

insulin resistance and improving insulin

sensitivity. Other suggested mechanism of

actions are:

a. by reducing white adipose tissue mass and

increasing brown adipose tissue mass.

b. by decreased production of TNF alpha,

leptin, and FFA levels in adipose tissue, all

of which cause insulin resistance.

3. In Muscle:

Troglitazone [1] increases GLUT-4 and

increases the activity of glycogen synthase.

There is increased glyucogenesis and glycolysis.

4. In Liver:

Thiozolidinediones reduce hepatic glucose

production by suppressing neoglucognesis. This

is by restoring the ability of insulin to suppress

the expression in the liver of PEPK

(phosphoenolpyruvate carboxykinase) the rate

limiting enzymes of gluconeogenesis.

5. Thiozolidinediones have been suggested to

decrease hyperglycaemia in activating

protoinkinase which reduces kinase activity of

insulin receptor.

6. Troglitazone reduces triglyceride level and

NEFA. It also decreases cholesterol, increases

HDL and to a lesser extent increases LDL level.

7. Troglitazone has no effect on body weight.

Safety data and Adverse Events:

Were reported from 30 clinical trials and 74000

weekly patient exposur to Troglitazone.

a. No hypolglycaemia occurs with Troglitazone

when used alone.

b. 2 to 3 % reduction in haemoglobin level with 5

to 7% elevation in plasma volume have been

reported. Hb% level did not fall outside the

normal range.

c. Liver Enzyme Activity increased to more than

3 fold of normal in some patients on

Troglitazone treatment. Varying degrees of liver

damage have been received by US, FDA. This

include irreversible damage and death in one.

This is probably an idiosynerotic reaction.

Prescribing Information

Troglitazone is metabolised by the liver and

excreted into the bile. The presence of renal

insufficiency does not effect the serum level or

metabolism of the drug.

1. In Type 2 diabetics, this is accompanied by

concomitant reduction in both fasting and post

prandial insulin levels. There will be significant

reduction in triglyceride level and an increase in

HDL cholesterol level. Dosage is 200-600

mg/day average dosage is 400 mg/day. Dosage

is once per day with breakfast and tiration is not

necessary.Troglitazone may be started either as

monotherohy or in combination with

INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 27

sulphonylureas, acarbose, metformin and with


2. In poorly controlled Type 2 diabetics on insulin

therapy, the insulin dosage reduction is not

recommended at the outset. Along with insulin,

troglitazone therapy is started. Once fasting

blood sugar falls to 120-140 mg a reduction of

10 to 20% of insulin dose is recommended in

order to aviod hypoglycaemia. Some studies

have reported (I) a reduction of insulin dosage

upyo 58%, (ii) reduction of insulin injection

from three to one per day in 40% of diabetics

treated with Troglitazone and (iii)

discontinuation of insulin in 10% of diabetics.

3. Troglitazone is the ideal drug for syndrome X

and other insulin resistant states.

4. In IGT :

In patients with IGT, Troglitazone decreases

insulin resistance and improves insulin

sensitivity,. It reduces insulin level and

normalises blood glucose level and prevents or

postpnes onset of Type 2 DM.

5. In Women with Polycstic Ovary Syndrome

with IGT :

Trogilazone improves glucose tolerance ,

insulin sensitivity and causes a fall in androgen

level Plasaminogen activiator inhibitor – 1

(PAI-1) level also falls (a prothrombotic factor).

Advantages of Troglitazone :

1. Once a day dosage

2. No dosage titration

3. No hypoglycaemia when used alone

4. No weight gain

5. Can be used along with sulphonyulurea,

Metformin and Insulin.

Hidden Benefits of Troglitazone:

1. Decrease in systolic, diastolic and mean blood


2. Decrease in triglyceride level. This means (1+2)

indirectly a reduction in anti-hypertensive and

triglyceride lowering drugs.

3. Decreases PAI-1 level, a prothrombotic factor.

4. May prevent or delay beta cell exhaustion.


Whatever be the benefits, while on Troglitazone,

patients liver enzymes are to be checked

periodically once a month initially and once in three

months subsequently. If the enzymes values are

more than three times of the normal value, the drug

should be discontinued at once.

For Further Reading:

1. Steven V. Edelman. Troglitazone: A new and unique oral

antidiabetic agent for the treatment of Type 2 diabetes an

the insulin resistance syndrome. Clinical Diabetes. 1997;


2. Traglitazone may cause irreversible liver damage. News –

The Lancet 1997; 350: 1451.

3. Bailey CJ, Williams G, Pickup J. New Drugs in the

management of diabetes and its complications. In the Text

Book of Diabetes. Ed. Pickup J and Williams G.

Blackwell, London 1997; 84.5-6.


Beta Cell Secretory defect, namely the insulin

deficiency is an important factor in the pathogenesis

of Type 2 diabetes, particularly during later stages

of the disease. As the disease progresses, there is:

1. Loss of sensitivity of insulin secretion to a rise

in blood glucose concentration and

2. Impaired processing of pro-insulin.

Insulin secretagogues provide useful therapeutic

approaches if used early in the natural history of the

disease. An ideal insulin secretagogue would restore

beta cell sensitivity to glucose and at the same time

ensure adequate biosynthesis, processing and

secertion of insulin to other nutrients, hormones and

neural factors. Insulin secretagogues can be divided

into (i) Initiators of Insulin secretion eg. Glimepiride

and Repaglinide; (ii) Potentiator of insulin secretion

eg. GIP and GLP –1 (Gastric Inhibitory polypeptide,

Glucagon Like Peptide).


Glimepiride is a newer, novel second generation

sulphonylurea. It increases insulin secretion by

stimulating beta cells and also has significant

extrapancreatic activity.

INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 28

1. Beta Cell Action:

Glimepiride binds to a specific receptor site 65 KDs

region in the beta cell while glibenclamide binds to

140 KDs region. Glimepiride binds to its receptor

2.5 to 3 times faster and dissociates from it binding

site 8 to 9 times greater than glibenclamide.

The mechanism of insulin secretion and release is

similar to gibenclamide ie. via the closure of ATP

dependent potassium channel and opening up of

voltage dependent calcium channel and increase of

intracellular calcuim concentration leading to

exocytosis of insulin.

Sulphonylureas act at the level of potassium – ATP

channel. However current sulphonylureas may not

stimulate beta cells in a controlled fashion or in

propotion to the blood glucose level, because of

their fixed blocking of potassuim-ATP channel.

Agents that accomplish this in a more flexible

fashion may lead to less secondary failure.

Glimepiride which binds to a differenct portion of

sulphonylurea receptor, leading to less fixed

blockage of potassium-ATP channel may have less

secondary failure.

The amount of insulin secretion is more or

equivalent to that of glibenclamide but the secretion

with glimepiride is very quick and lasts for a short

time than glibenclamide and hence there will be no

hyperinsulinism and reduced likelihood of inbetween

meal hypoglycaemia.

2. Insulin-independent blood glucose decreasing

activity of Glimepiride: (Extra-pancreatication):

Glimepiride exhibits a more pronounced insulin

independent blood glucose decreasing activity

compared to glibenclamide. This can be explained

by stimulation of glucose transport and nonoxidative

glucose metabolism and adipose tissue

and muscle cells. The increased glucose transporter

activity is brought out by increased translocation of

GLUT-4 isoform from inside the cell to surface of

adipocytes and muscle. It increases insulin

sensitivity and decreases insulin resistance. If

hyperinsulinemia is a concern in therapy of Type 2

diabetes, the higher insulin-independent blood blood

glucose decreasing activity of glimepiride might be

of therapeutic relevance.

Thus the more pronounced blood glucose decreasing

activity of glimepiride is brought out by its quick

insulin release in conjunction with an insulinindependent

glucose decreasing activity at the


The extra pancreatic effects of glimepiride may

explain the lesser degree of insulin stimulation for a

given fall in blood glucose, in both short term and

longer clinical studies compared with other

sulphonylureas. In vitro, glimepiride stimulates

glycogen formation, glucose transport and other

insulin like effect. It decreases hepatic


There is not much difference in absorption whether

glimepiride is given just before or along with food.

The peak concentration of the drug is attained in one

hour. The half life of the drug is 9 hours. The drug is

100% bioavailable. It has dual mode of excretion

40% through liver and 60% through kidney. The

metabolites are not much active.

The quick insulin release, increased peripheral

tissue glucose disposal and the peak action at one

hour are responsible for smooth control of postprandial

hyperglycaemia. The prolonged half life

suggests that once daily dosing of glimepiride is

enough to maintain blood glucose control for 24


Efficacy wise glimepiride is equivalent to that of

glibenclamide. It decreases both fasting and post

prandial hyperglycaemia. The HbA1c decreases 1 to

2% within three months with 1 to 2 mg dose. The

fall in HbA1c is upto 3.5% when the drug is initiated

in diabetics with HbA1c more than 10.5%. There is

no increase in fasting C – peptide and insulin levels

even upto one year of treatment.

The hypoglycaemic episodes are very few in

number, lesser in intensity and are of shorter

duration. The hypoglycaemic episodes vary from

0.9 to 1.7% when compared to glipizide and

glibenclamide, both of which cause more severe

hypoglycaemic episodes.

Glimepiride safeguards the physiological

suppression of endogenous insulin release during

active physical exercise, implying that post exercise

induced hypoglycaemia may not occur with the


It has been observed in animal studies that platelet

inhibitory effect of glimepiride is much more

pronounced than gliclazide and hence it may have a

preventive effect in the development of

microvascular complications.

Dosage and Administration:

INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 29

Glimepiride is indicated in Type 2 diabetics when

diet and exercise fails. Dosage is individualised for

each patient so as to achieve and maintain

satisfactory blood glucose level at a minimum

effective dose. The fasting blood glucose and

HbA1c measurements should be performed


The usual starting dose of glimepiride is 1 mg.

Maximum initial dose 2 mg once daily taken just

before breakfast or with the first main meal of the

day. Further increments can be made at 1 or 2 week

intervals in increments of 2 mg. The patient’s blood

glucose response should guide dosage titration. The

usual maintenance dose is 1 to 4 mg once daily.

Maximum recommended dose is 8 mg once daily.

There is no need to split the dosage to twice daily.

Once daily dosage will improve patient’s


Combination Therapy with Insulin :

For patients with secondary failure to other

sulphonylureas when glimepride and insulin therapy

is indicated, the recommended dosage of

glimepiride is 8mg once daily, Insulin is then

titrated from a low dosage upward with

approximately once-weekly dose increase guided by

fasting blood sugar measurements. Glimepiride

lowers daily insulin dosage requirements.

In Special Populations :

In American clinical trials, tight control ie. HBA1c

levels of 7.2% or lower was achieved in 68% of

obese diabetics and in 78% of diabetics with


No marked difference in the safety profile and daily

dosage were observed between patients who were

young and elderly, obese and non-obese, male and

female and among patients of various racial


Glimepiride has less effect on cardiovascular system

than do glyburide and glipizide and has decreased

binding to cardiovascular ATP dependent potassium

channel causing one-third the degree of inhibition

seen with glyburide. There is also less alteration of

coronary blood flow. Thus interestingly, glimepiride

appears to be "Pancreas Specific" in its effect on the

potassium-ATP channel and hence it could be used

in cardiac patients with mild to moderate


Glimepiride should not be used in pregnancy and in

lactating mothers.

No clinically significant drug interactions were

observed with commonly used drugs such as

calcium channel blockers, ACE inhibitors, H2

receptors antagonists, fibrates, NSAID,

sympathomimetic agents, sulphonamides and

thyroid hormones.

Clinical studies indicate that glimepiride offers

significant benefits in the management of Type 2


1. It has the greatest (mgm. for mgm.) glucose

lowering effect when compared to other


2. It achieves tight control in more than two thirds

of the patients.

3. It maintains effective control upto 2 1/2 years .

4. It reduces insulin resistance and has a unique

beta cell receptor binding capability.

5. Once daily dosage will improve patients


6. It has insulin sparing activity. Glucose levels are

controlled without meaningful increase in

fasting insulin and in Type 2 diabetics requiring

exogenous insulin, glimepiride lowers daily

insulin dosage requirements.

For Further reading :

1. ZT Bloomgarden, New and Traditional

Treatment of Glycaemic in NIDDM. Diabetes

Care. 1996; 19:295 – 9.

2. Ronald B Goldberg, A dose response study of

Glimepiride in patients with NIDDM who have

previously received Sulphonylurea Agents.

Diabetes Care. 1996; 19 : 846-56.

3. Muller G. The Sulphonylurea --- Glimepiride ---

Diabetes 1993;42 : 1852-67.

4. Bailey CJ, Williams G, Pickup J. New drugs in

the management of diabetes and its

complications. In Text Book of Diabetes Eds.

Pickup J and Williams G., Blackwell, London,

1997; 84.8-11.

5. A Monograph on Glimepiride by Hoechst

Marion Roussel.



INT. J. DIAB. DEV. COUNTRIES (1998), VOL. 18 30

Repaglinide is a non-sulphonylurea antidiabetic

agent and a short acting insulin secretagogue. It is a

benzoic acid derivative and is an analog of

meglitidine family.

The meglitidine shares the non-sulphonylurea

moiety of glibenclamide.


Repaglinide has a unique binding site on beta cell,

different from that of glibenclamide. It acts via

closure of ATP dependent K channel in beta cell. It

to 3 to 5 times more potent insulin releaser than

glibenclamide but its action is short lived. The half

life of the drug is 2.5 hours and peak action is less

than one hour. It reduces post-prandial blood sugar

by 4 to 6 mmol and HbA1c by 2%. It is metabolised

in the liver and secreted in bile.

Repaglinide vs Glibenclamide:

When compared to glibenclamide, Repaglinide has

the following characteristic feature:

1. Fast Absorption

2. Short biological half life

3. Short duration of insulinotrophic activity

4. Lowest post-prandial Blood glucose

5. No in-between meal hypoglycaemia or


Uses :

a) Primary Therapy in Type 2 Diabetes

Repaglinide is a prandial glucose regulator. It has a

fast onset and short duration of action. The initial

dose is 0.5 to 1 mg and gradually increased upto 2 to

4 mg. It should be administered three times a day

just, before along with or immediately after a meal

and offers greater flexibility in meal times and drug


b) Useful in patients who eat at irregular times

or miss a meal:

Repaglinide increases insulin secretion sufficient to

control the post meal surge and not for so long as to

produce hypoglycaemia in-between meals and

especially when a meal is missed or delayed as is

the case with long acting insulinotrophic agents. So,

there is no in-between meal hypoglycaemia and

there is no in-between mean hyperinsulinemia.

The Other Notable Features of Repaglinide

Actions and Uses are:

1. The intermittent stimulation of K channel that

prevents down-regulation of receptors and

consequent refractoriness and secondary failure

of therapy.

2. It has no effect on ATP-regulated K channel of

cardiocytes or vascular smooth muscle cells

(Landry D. L. Oliver, Jan. 1992) and therefore

may be preferable to compounds that produce

this effect.

3. Rapid non-renal inactivation and elimination

results in a shortswift, "Antihyperglycaemia"

action. So, it can be administered safely in

patients with compromised early renal or

hepatic function.

Combination Therapy : Regaplinide and


Repaglinide acts only at beta cells leading to insulin

release, whereas metformin bypasses beta cell and

acts at periphery, liver, muscle and adipose tissue.

The actions are complementary to one another,

when both the drugs are combined. The fall in

HbA1c is significant within three months in most

Type 2 diabetics.

For Further Reading:

1. A D AAnnual Meeting 1997, Type 2 Diabetes, Diabetes

Care 1997 : 30(11): 1791-5.

2. A. Gradul et al Repaglinide, Drugs of the Future 1996 :

21(7): 694-9.

3. Malaise W. J. Stimulation of Insulin release by Non-

Sulphonylurea Hyperglycaemic agents – Hormone and

Metabolism Research 1995 : 27 :263-6.

4. Novo Nordisk Diabetes Update – 1997 & 1998.

my contact

19 Replies

Very scientific,elaborate and educative and valuable as reference material.As a layman,I request you to kindly give specific advise that I can put to practical use.

veerendras in reply to Hidden

This being information about the Diabetes and drugs and response of med . here in form the system is like that if any thing is given specific with addresses members of forum has objections since when explanation is given like wise ref mentioned the specific names may come

Doctor of your choice may be selected by you shall be able to give info

sir meaning of long whaeat is not clear if you can attach a picture to me direcly at may be it is same -the one in my mind

Thanks and regards

Pictures of long wheat & ordinary wheat are at

Thanks for appreciation


I am indeed consuming long wheat porridge for breakfast and getting positive results.I have developed a liking for it.

veerendras in reply to Hidden

is it barley or what since I did not find it in market

Hidden in reply to veerendras

Please open the link below.It gives you information on the subject provided by SHOOTERGEORGE,one of the learned bloggers on this site.

In Bangalore it is available in NILGIRi'S store and it is called Samba wheat

veerendras in reply to Hidden

Thanks I got reply also Jau/Barley is the same -Thanks again for supporting

Hidden in reply to veerendras

It is "Jau" in Hindi - available in local kirana stores with or without the husk. I have tried it myself and like the taste as well.

ShooterGeorge in reply to Hidden

You are right. Thank you venkas1.

veerendras in reply to Hidden

Thanks a lot sir


ShooterGeorge in reply to Hidden

Hi venkataramana,

That is a glad news to me; keep it up. Long Wheat is really tasty & has enough carbohydrate in it. In addition, it will cure diabetes.

but sir carbohydrate intake is to be restricted / eg LCHF diet recommendations and others

Hi veerendras,

Carbohydrate intake restriction will obviously bring down sugar level. It is simple & straight forward. "Will it cure Diabetes" is the question. Bringing down blood sugar to normal level is NOT curing. Until I confirm (with the set of four standard tests) for at least ONE CASE, I will not say "yes".

Sir thank you for the link


Hi veerendras,

Did you see the photographs at ? If you had clicked on the pictures, they would have been enlarged. Then you could have seen it in actual size or slightly larger. Either do that OR

Click the following links. First link will show you Long wheat collection and second link gives a comparison picture of ordinary wheat, Long wheat, Long wheat with husk & tip of a dot pen for size comparison.

Even after seeing those if it is not clear, give me your postal address to send a small quantity of it.

Wish you all the best.

Dear Sirs

The things are clear and really salute to you for the record and presentation made

In case if I will difficulty I will get in touch

Thanks once again

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