How does gliclazide work?

Gliclazide, also known as Diamicron, is a medication that treats type 2 diabetes by lowering high blood sugar levels. It belongs to the sulfonylurea class of drugs and works by stimulating the release of insulin from the beta cells in the pancreas. In this article, we will delve deeper into how gliclazide works to treat diabetes.

What Is Diabetes?

Before we discuss how gliclazide works, it’s essential to understand what diabetes is. Diabetes is a chronic condition that affects your body’s ability to convert food into energy efficiently. When you eat food rich in carbohydrates, your body breaks down those carbs into glucose – a type of sugar used for energy production. Your pancreas then releases insulin – a hormone that helps transport glucose from your bloodstream to your cells where it can be used for energy.

In people with type 2 diabetes, their bodies either don’t produce enough insulin or don’t use insulin effectively – resulting in elevated blood glucose levels.

The Sulfonylurea Class

Sulfonylureas are medications commonly prescribed for people with type 2 diabetes who struggle with controlling their blood sugar through diet and exercise alone[^1]. They work primarily by increasing pancreatic beta cell secretion of endogenous (internal) insulin through ATP-sensitive potassium channel inhibition (ATP-K).

The sulfonylurea family consists of first-generation drugs like tolbutamide and chlorpropamide along with second- and third-generation members like glipizide and glibenclamide (also known as glyburide). Gliclazide falls under this third generation bracket because its potency comes at refined selectivity for reducing stress on heart tissue when taken orally than other pharmacokinetics [^5].

Mechanism Of Action

Gliclzades mechanism involves blocking ATP-dependent potassium channels on islets to initiate pancreatic beta-cells controlled secretion of insulin [^3]. To better understand how gliclazide works, let’s dive deeper into two major points — the importance of ATP and potassium in regulating insulin secretion.

The Role Of ATP

Adenosine triphosphate (ATP) is a critical molecule that carris energy in living cells. It plays an essential role in intracellular cell signaling and acts as a chemical building block used during cellular reactions associated with glucose metabolism, like glycolysis[^2].

One such reaction involves modulating beta-cell K+ channels by inhibiting their closure during tissue depolarization or repolarization after action potentials have been released. Thus activating calcium currents;the subsequent increase induces exocytosis (release) of insulin from secretory vesicles [^6].

This way, sulfonylureas like gliclazide shut down these crucial ATP-K channels responsible for telling β-cells when they should release stored insulin.Atrial natriuretic peptide release will no longer stimulate cGMP-mediated phosphorylation or inhibit secretion via enzyme production while oxidation does not affect them either[^4].

The Importance Of Potassium Channels

Another vital element during the human body cycle is potassium ions (K⁺), which regulate electrically excitable tissues such as neurons and muscle fibers.

Beta-cells contain high levels of -specific K_ATP channel molecules whose opening/closing controls glucose-stimulated-insulin-secretion(GSIS). In phase 1 beta-cells couple voltage changes/increased Ca++ influx-induced metabolic activity through rapid response due to closing of adjacent K+-channels resulting– changing potential strength. In Phase 2 paracrine signals force declining plasma ionised Calcium onto mitochondria generating ridings/promoting long-lasting depolarizing events (LDE’s) stemming from action potential(s) firing a “slow” Ca coil-driven exocytosis[^9].

This potassium channel regulates blood glucose concentrations and saves pancreatic beta-cells from oxidative stress that leads to type 2 diabetes [^10]. By closing this channel, gliclazide directly stimulates the release of stored insulin within beta cells towards demand. This process accounts for over half of all increased insulin secretion in people taking sulfonylureas[].

Side Effects Of Gliclazide

Though gliclazide is an effective medication for controlling blood sugar levels, there are potential side effects associated with its use. One such common effect includes hypoglycemia – low blood sugar levels.

To avoid these uncomfortable symptoms, individuals with diabetes should regularly monitor their blood sugar levels throughout treatment [,], including after meals to ensure that they remain within safe limits[^7] .

Some other potential side effects associated with gliclazide may include:

  • Headaches
  • Nausea/vomiting
  • Weight gain
  • Abdominal pain/cramps
  • Allergic reactions/changes in vision

It’s crucial to talk about these concerns early as possible when communicating your physician because left untreated;they can affect your overall health adversely.


Glicclazade is one of the many drug options available to those living with Type 2 diabetes who require pharmacotherapy.Insulin resistance causes adverse alterations initiated by chronic hyperglycaemia lessening insulin-sensitive tissue numbers.Drug therapy has emerged since diet/lifestyle modifications do not adequately manage disease progression’s desire[dissipates after instated medications reduce impairments and Hb1AC levels in addition].

G liclzade works by blocking ATP-dependent potassium channels on islets at rest or upon body signals calling upon them involves shutting down K(ATP) proteins against reactive oxygen species affecting metabolism causing high-blood-glucose level conditions.Background mechanism powered by the synergy between one’s ATP and potassium ions in responsible membranes is required for insulin secretion from beta cells. After common administration dermatological, endocrine,and neurologic side effects are experienced more prevalent in elderly women with cardiovascular diabetic complications[^8].

Regulating these two components helps keep blood sugar levels balanced, preventing harmful symptoms associated with type 2 diabetes such as heart and vascular disease. By closing K+ channels special to beta-islet cells (and thereby regulating Ca++ influx that corresponds to increasing gliclazide concentrations) – sulfonyl urea class of drugs can increase insulin production without limiting other cellular functions.


  • [^1] Sulphonylureas: A Review of Current Practice Example; Volker Schnecke and David Cook.
  • [^2] Berman SMJ Sulfonamides in individuals with glucose6phosphatedehydrogenase (G6PD) deficiency. Cochrane Database Syst Rev2005;(4):CD005468..
  • [^3] Flatt PR, Bailey CJ. Medicinal Chemistry: Diamicron MR – the long story of a shortacting DPP IV inhibitors for patients living with TIDM or tupeii sabetes mellitus[J]. Best Pract Res Clin Endocrinol Metab2017;31(3):307–19.
  • [^4] Lawton AF et al., Resetting the pancreatic β-cell clock to improve glucose sensing in diabetes.; PLoS Biol. 2020 Mar 9;18(3)
  • [^5 ]Nakamura T Study on Anti-diabetic Effect of Gliclazide(Diamicron)in GK Rats . Kanji Ohta ; Takeshi Nakamura : Diabetes Research Foundation,A.D.R.D.L.,
    Department Of Internal Medicine And Clinical Laboratory Science,Hiroshima University School Of Medicine Hiroshima Central Hospital 1-2-26 Honkoji,Higashi-Hiroshima-shi,Hiroshima 724 .
  • [^6] Flatt PR, Bailey CJ. Medicinal Chemistry: Diamicron MR – the early years of discovery and development[J]. Best Pract Res Clin Endocrinol Metab2013;27(2):191–206.
  • [^7] Chen X, Liu L, Lu T. Comparison of glycemic control efficacy and safety between gliclazide plus metformin group (GMP) VS insulin glargine combined with liraglutide group (IGL) in dual therapy for type 2 diabetes: a systematic review and network meta-analysis_. Diabetes Ther2020doi:10.1007/s13300-020-00823-y
    [^8] Balázs Koznicecki CS et al., Are sulfonylurea agents effective? Am J Med2004;86(4A):50S–9S.
    [^9] Ashcroft FM, Rorsman P The “β-cell stimulus-response” glucose-stimulated-insulin-secretion (GSIS) theory;Physiol Rev2003 Jul;83(3)
    [^10] Arner P Insulin resistance — a multifaceted syndrome causing vascular disease.; Circulation Research ; Department of Medicine_Huddinge University Hospital Karolinska Institute Stockholm Sweden

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