#diabetes #heartfailure #kidneydisease #empagliflozin #jardiance #chronickidneydisease #chronickidneyfailure #type2diabetes #metformin #modeofAction #moa
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Empagliflozin +Metformin | Mode of Action and Latest treatment for #diabetes #heartfailure #kidneyfailure #weightloss #obesity Treatment and Benefits
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The human kidney is involved in the regulation of glucose homeostasis and in abnormalities found in diabetes mellitus via three different mechanisms: release of glucose into the circulation via gluconeogenesis; uptake of glucose from the circulation to satisfy its energy needs; and reabsorption into the circulation of glucose from glomerular filtrate.
Macula densa cells are renal sensor elements play an important role in regulating glomerular filtration rate and blood flow.
The vast majority of glucose filtered through the glomerulus is reabsorbed within the proximal tubule, primarily via SGLT2 (sodium-glucose linked co-transporter-2)
It is found almost exclusively in the proximal tubules of nephronic components in the kidneys. SGLT-2 accounts for about 90 percent of glucose reabsorption into the blood. sodium , potassium ATPase on the basolateral membrane of proximal tubular cells utilize ATP to actively pump sodium ions into the interstitium surrounding the tubule, establishing a sodium gradient within the tubular cell.
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SGLT2 on the apical membrane of these cells then utilize this gradient to facilitate secondary active co-transport of both sodium and glucose out of the filtrate, thereby reabsorbing glucose back into the blood – inhibiting this co-transport, then, allows for a marked increase in glucosuria and decrease in blood glucose levels.
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Empagliflozin is a potent inhibitor of renal SGLT2 transporters located in the proximal tubules of the kidneys and works to lower blood glucose levels via an increase in glucosuria
The vast majority of glucose filtered through the glomerulus is reabsorbed within the proximal tubule, primarily via SGLT2 (sodium-glucose linked co-transporter-2)
It is found almost exclusively in the proximal tubules of nephronic components in the kidneys. SGLT-2 accounts for about 90 percent of glucose reabsorption into the blood. Na+/K+-ATPase on the basolateral membrane of proximal tubular cells utilize ATP to actively pump Na+ ions into the interstitium surrounding the tubule, establishing a Na+ gradient within the tubular cell.
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SGLT2 on the apical membrane of these cells then utilize this gradient to facilitate secondary active co-transport of both Na+ and glucose out of the filtrate, thereby reabsorbing glucose back into the blood – inhibiting this co-transport, then, allows for a marked increase in glucosuria and decrease in blood glucose levels.10
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Metformin’s mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production, decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization. It is well established that metformin inhibits mitochondrial complex I activity, and its potent antidiabetic effects occur through this mechanism.
thereby inhibiting fat synthesis and leading to fat oxidation, reducing hepatic lipid stores and increasing liver sensitivity to insulin.
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Approved medicines in the SGLT2 inhibitor class include:
Brenzavvy™ (bexaglifloxin)
Invokana® (canagliflozin)
#Farxiga ® (dapagliflozin)
#Jardiance ® (empagliflozin) #jardines
Steglatro® (ertugliflozin)
Dosage Forms & Strengths
tablet
10mg
25mg
Type 2 Diabetes Mellitus
Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes (T2DM)
Also indicated to reduce the risk of cardiovascular death in adults with type 2 diabetes mellitus and cardiovascular disease
10 mg PO qDay
May increase to 25 mg/day if needed and tolerated
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Heart Failure
Indicated to reduce the risk of cardiovascular death plus hospitalization in adults with heart failure (HF)
10 mg PO qDay
Chronic Kidney Disease
Indicated to reduce risk of sustained decline in eGFR, end-stage kidney disease, cardiovascular death, and hospitalization in adults with chronic kidney (CKD) disease at risk of progression
10 mg PO qDay
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