Prophylactic Effect Of Caffeine Towards Type 2 Diabetes

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Abstract:

Type 2 diabetes accounts for about 95% of total diabetic individuals. Its prevalence is increasing these days. This article revises the effect of
caffeine on type 2 diabetes and its mechanisms. Type 2 diabetes is characterized by two conditions: insulin resistance and β cell dysfunction leading
to reduces insulin secretion. It results in increased postprandial glucose levels which lead to hyperinsulinemia and hyperglycemic condition. There are
various factors which accounts for this condition like increase in free fatty acids, decreased glucose uptake, genetic modification, increased glucose
production (HGP). Caffeine being a stimulatory substance found to reduce the risk of type 2 diabetes. There are various mechanisms accounting for this
action: mobilization of calcium, inhibition of phosphodiesterase and antagonism of adenosine receptors. Also the studies have proven to have reversal
effects with chronic usage of caffeine.

Key words
: Type 2 diabetes, β cell Dysfunction, Insulin Resistance, Postprandial glucose levels, Hyperinsulinemia, Phosphodiesterase.

Introduction:

Type 2 Diabetes

Type 2 diabetes is complex, heterogeneous and involves multiple etiologies. It is also called as Non-Insulin Dependent Diabetes Mellitus (NIDDM). It is
characterized by two conditions: Insulin resistance and Beta cell dysfunction. The prevalence of the disease is increasing drastically all over the
world due to sedentary life style and consumption of high fat and carbohydrate content diet. According to Andrew J. Krentz, Clifford J. Bailey (2005)
and F.Belfoire, S.lannello (2000), this disease accounts for 95% of total diabetics. This prevalence varies from country to country. According to the
Diabetes Atlas 2006 which was published by the International Diabetes Federation, the number of people with diabetes in India presently are 40.9
million and estimated to be 69.9 million by end of 2025..According to WHO Expert Committee on Diabetes (1980),powerful risk for Type 2 Diabetes is
obesity.

Pathophysiology :

In normal conditions, after glucose load, there will be release of insulin from Beta cell due to increase in glucose levels. The released insulin acts
on α-subunit and causes signal transmission to β-subunit which activates tyrosine kinase.This enzyme suppresses the High Glucose Production (HGP) and
stimulates the glucose uptake by the skeletal muscle and adipose tissue. Glucose homeostasis is carried by three processes in body: Insulin secretion,
stimulation of glucose uptake by splanchinic and peripheral tissues & suppression of high glucose production (26). Fasting glucose levels reflects
the HGP and insulin sensitivity.

But in type 2 diabetics slightly diminished binding activity of insulin to α-subunit is seen. Due to this there is increase in glucose production (HGP)
and impaired glucose uptake. In these individuals elevated fasting glucose levels are seen due to increase in glucose production and hyperinsulinemia.
According to Bulanga L. Nyomba, in these individuals the glucose metabolism in response to insulin is reduced by 40%. An initial stage of type 2
diabetes is characterized by increase in postprandial glucose levels resulting in islet cell hypertrophy (31).

Type 2 diabetic subjects have multiple deficiencies in insulin activity: impaired binding and activation of receptor, impaired phosphorylation of β-sub
unit, impaired translocation of GlUT-4 to cell surface (released in response to insulin release and involved in glucose uptake) and impaired incretin
release(31).

Insulin resistance:

It is the initial stage in development of disease and initiates 5-10 years prior. This condition is due to high glucose production(HGP) and fasting
hyperinsulinemia.Insulin resistance is developed due to following reasons(4,27,31): Release of Free Fatty Acids(FFA) from adipose tissue, impaired
glucose uptake (diminished translocation of GLUT-4 leading to hyperglycemia) and rise in levels of inflammatory mediators like C- Reactive
protein,Interlukin-6 (involved in adipocyte signaling) &Tumor necrosis factor-α. An increased level of Interleukin-6 is seen mainly in obesity
conditions due to functional gene variations (38).

Enlarged fat cells are resistant to antilipolytic effects of insulin and increases the plasma free fatty acid levels and thus stimulates
gluconeogenesis, hepatic and muscle insulin resistance and leads to lipotoxicity.These dysfunctional fat cells causes inflammation and atherosclerosis
leading to condition which fails to secrete normal insulin sensitizing cytokinesis (25).According to Boden and Shulman(2002), increase in free fatty
acid and intracellular lipid levels inhibits insulin signaling and produces diminished translocation of GLUT-4 to cell surface. This high level of
fatty acids leads to hyperglycemia in liver which antagonizes the action of insulin on endogenous glucose production.

β-cell dysfunction:

β-cell dysfunction is due to delay in first phase insulin resistance. Hyperglycemic condition results due to deterioration of β-cells which worsens the
disease. Even accumulation of free fatty acids in pancreatic islets reduces the mass of β cells and results in this condition(Unger and Zhou,2001).
There are two proposed possible mechanisms for β-cell dysfunction (10, 35): Genetic modifications in gene MODY (Maturity Onset of Diabetes of Youth),
Glucotoxicity and lipotoxicity due to hyperglycemia and increased free fatty acid levels.

Caffeine

Discovery of caffeine:

According to Henry watts (Dictionary of chemistry, 1863), the scientific history of caffeine began in 1819.Friedlieb Ferdinand Runge, a young
physician, discovered and isolated the caffeine in 1819 using paper chromatography technique. It was an accidental discovery when he was preparing the
medicine from belladonna plant a drop fell into his eyes and led to pupil dilation and blurred vision.

Sources of caffeine:

Caffeine is mainly distributed in tea, coffee and coca plants. The percentage of caffeine differs in these sources (Table-1).Caffeine commonly found in
the complex form with chlorogenic acid and proposed that it was formed during the extraction process (1).

Properties of caffeine:

Caffeine is member of xanthenes family. Chemically, it is 3, 7-dihydro, 1, 3, 7-trimethyl, 1H-purine, 2, 3-dione. Molecular formula of caffeine is
C₈H₁₀N₄O₂ and molecular weight is 194.1906 Daltons. Caffeine is odourless, bitter and white fleecy powder or prismatic crystals. It is fat soluble and
freely soluble in hot water. It sublimates at 458˚F.

Pharmacology of caffeine

Caffeine has mild central and respiratory stimulant properties. It readily distributes throughout body even crosses blood brain barrier. High doses of
caffeine cause tachycardia and increases coronary blood flow. It also has diuretic actions and increases gastric stimulation. The main mechanisms of
caffeine action are: mobilization of calcium, inhibition of phosphodiesterase activity and antagonism of adenosine receptors.

Caffeine And Type 2 Diabetes

Caffeine intake was found to reduce the risk of type 2 diabetes (14, 15, 17, 37). It was found that caffeine intake of 416mg/d reduced the risk by 33%
mainly among men with BMI (Basal Metabolic Index) of 25kg/m or greater but not lesser (15).

Inhibitory action of caffeine on phosphodiesterase enzyme:

Glucose when co-administered with caffeine resulted in high exogenous carbohydrate oxidation due to increased intestinal glucose uptake. This was
mainly due to inhibition of phosphodiesterase activity which enhances the activity of SGLT-1 (responsible for carbohydrate oxidation) and this was
found to be higher during exercise. In late 1950’s this activity of inhibiting the phosphodiesterase enzyme was discovered (Rall and sutherland, 1958).
Inhibition of this enzyme delays the cAMP metabolism. This activity of caffeine was found to be responsible for glucose uptake and metabolism of
endogenous compounds .i.e., carbohydrate and fat oxidation. The activity of metabolism of endogenous compounds was found mainly due to modification
in genes CYP6a₂ and CYP56a₃ and this was mainly found in Drosophila melanogaster.(6). Fat oxidation reduces the plasma free fatty acid levels which
reduces the gluconeogenesis thus reduces the glucose production in liver and enhances the insulin sensitivity. As the increased levels of free fatty
acids are responsible for diminished translocation of GLUT-4 which reduces the glucose uptake (Boden and Shulman, 2002), reduction of free fatty acid
levels also results in increased glucose uptake.

Even this inhibition of phosphodiesterase enzyme of caffeine is responsible for the activity of caffeine on gastric emptying, liver glucose disposal,
muscle glucose uptake, cardiac stimulation, vasodilatation, bronchodilation, increased blood levels of ACTH, corticosteroids (20, 37). These actions
differ in lean and obese patients.

Caffeine’s action on Ryanodine (RY) receptors:

Regular caffeine intake also found to increase blood pressure upto 2-3 fold. This effect was found both in men and women but due to different
mechanisms. In men the increase in blood pressure is due to different hemodynamic mechanism .i.e.; increase in vascular resistance and in women it is
due to increased in cardiac output. Reason for difference in mechanisms among men and women was not clearly known. This increase in blood pressure is
mainly due to mobilization of calcium which leads to increase in release of catecholamines (20, 23, 40). Caffeine causes mobilization of calcium due to
its action of Ryanodine(RY) receptors in pancreatic β cells and this was found to be main mechanism for which it enhances the insulin secretion and
also responsible for release of catecholamines from adrenal medulla(20).

The mobilization of calcium takes place in two steps: Firstly, small release of calcium, and secondly, released calcium acts on RY receptors which
cause calcium dependent release of calcium from sarcoplasmic reticulum.

It was found that low doses of caffeine (0.5-2.0mM) sensitizes the RY receptors for the calcium entry and causes calcium dependent sarcoplasmic calcium
release and increases the frequency of opening of RY receptors. But at high doses it directly opens the RY receptors and causes calcium independent
calcium release mechanism.(16,21,29). Doses of caffeine differ with the age. As the age increases the dose also increases and adults are recommended to
take a dose of 400mg/day (Table-3).As caffeine is major constituent present in most of the beverages, consumption of these beverages also effects the
dosage of caffeine because the amount of caffeine present differs from one beverage to another and amount of caffeine was found to be high in coffee
about 30-150mg (Table-2).

Caffeine also increases the metabolic rate upto 70% and at dose of 100mg was found to increase Resting Metabolic Rate (RMR) by 3-4% which also
increases the Energy Expenditure (EE) in both post obese and lean patients (2, 18).

Studies also shown that the 12hour intervention of caffeine significantly increased aerobic capacity, decreased body weight, body fat, fasting glucose
level(13%), serum insulin levels(40%), C-peptide( C- Reactive protein-predictor of fasting insulin levels) (33%) and proinsulin concentration(12%).

Caffeine’s action on Adenosine receptors:

Caffeine also competitively inhibits the adenosine receptors. Adenosine is inhibitory neuromodulator which have mood depressing, hypnotic and anti
convulsant property. It induces vasodilatation, hypotension, bradycardia, decreased nerve firing and inhibits release of Nor Adrenaline (NA) (5).
Adenosine receptors are three types: A₁, A₂, A₃ where A₁ inhibits adenyl cyclase and calcium channels and stimulates potassium channels and A₂
stimulates adenyl cyclase. Caffeine at moderate doses (30-50µM) was found to inhibit tonic adenosine mediated (central) activation of A₁. Central
activity of caffeine is biphasic .i.e., low doses enhances alertness and elevates mood where as high doses causes restlessness and anxiety. Biphasic
effect of caffeine is due to co-relation of phosphodiesterase inhibition with behavioral depression (blockade of A₁ receptors) (20). According to
Boulengel et al (1983) and Fredholm (1982), chronic administration of caffeine for 7-14 days to rat increased the number of receptors.

The chronic administration of caffeine causes caffeine withdrawal syndrome which sensitizes the A₁ receptor adenylate cyclic system and down regulates
the β-adrenergic receptors (28). Even caffeine metabolite paraxanthine was found to be adenosine receptor antagonist (7). Somnolytic effects (Virus,
Ticho, Pildtich & Radulovacki, 1990) and epileptogenic effects (Moraidis and Bingmann, 1994) is due to blockade of adenosine receptor.

In contrast to above reports, Keijzers et al shown that acute caffeine ingestion resulted in decreased insulin sensitivity in healthy volunteers due to
increased plasma epinephrine and free fatty acid levels. Also it was found that there is significant reduction in glucose uptake in lean (25%), obese
non diabetics (26%) obese type 2 diabetics (36%) on caffeine ingestion. Blood glucose levels also increases during Oral Glucose Tolerance Test (OGTT)

Conclusion:

In summary there is reduced risk for type 2 diabetes with the caffeine usage and the exact mechanism for reducing the risk of type 2 diabetes was not
studied. The studies have not shown the effect of caffeine in type 2 diabetic patients-does it suppresses or worsens the disease? Also it is shown that
the acute effect of caffeine is shown to reduce the risk of type 2 diabetes but the reversal is seen with the chronic administration due to caffeine
withdrawal syndrome, the mechanism for reversal is yet to be studied. The mechanism for reducing the risk was not clearly explained. Even the amount of
caffeine varies with the beverage which also reflects its effect after consumption. But this concept is yet to be cleared.

From the above studies it can be seen that there is no direct action of caffeine on β cells. Rather caffeine reduces risk by releasing the
catecholamines and glucose uptake. Due to release of catecholamies there is increase in energy expenditure, contraction of muscle and increase in
resting metabolic rate. Due to increase in glucose uptake there might be the reduction of plasma glucose levels there by reducing the hyperglycemic
risk which is initial stage of type 2 diabetes. There is no evidence that whether the glucose uptake is due to increased signaling in GLUT-4
transporter or by mobilization of calcium. Apart from these various unanswered questions it is proved to reduce the risk of type 2 diabetes and acts as
a prophylactic effect.

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Table-1: It gives the information about the percentage of caffeine present in different sources (24).

Source

Common name

Part of the plant

Percentage of caffeine present

Family

Coffea arabica

Coffee

Seeds

1-2%

Rubiaceae

Camellia sinesis

Tea

Leaf dust

1-4%

Theaceae

Cola nitida, Cola accuminata

Cola

Seeds

3%

Sterculiaceae

Theobroma cacao

Cacao,Drind chocolate

Roasted seeds

0.2-0.5%

Sterculiaceae

Ilex paraguensis

Mate tree

Dried leaf

0.8-1.7%

Aquifoliaceae

Paullinia cupana

Guarana

Seeds

2%

Sapindaceae

Table-2 : It gives the information about amount of caffeine present in different beverages (24).

Beverage

Amount of caffeine present

Coffee

30-150mg (average of 60-80 mg)

Instant coffee

20-100 mg (average of 40-60mg)

Decaffeinated coffee

2-4mg

Tea

10-100mg (average of 40mg)

Cocoa

2-50mg (average 5mg)

Cola drink

25-60 mg

Table-3: It gives recommended intake of caffeine based on the age (9).

Individuals

Recommendations (mg/d)

Children

-

4-6years old

45.0

7-9 years old

62.5

10-12 years old

85.0

Adults

400

Pregnant/ breast feeding women

300

About author:

Nagasai Hema Sree Ganga

Nagasai Hema Sree Ganga

Sitha Institute of Pharmaceutical Sciences, # 8-5/4, Rajiv Gandhi Nagar, Bachupally, Hyderabad-500072. Ph.no:9705869936, 040-23043880. Email: nagasaiganga@yahoo.in, nagasai.hemasree615@gmail.com

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