One of the most critical biomedical discoveries of the 20 th century–insulin in 1921, overshadowed the use of other medications to treat diabetes ( 40). However, it did not come into broad use to treat diabetes initially. For the remainder of the paper, the use of Metformin assumes the use of Metformin HCl.Īdvances in chemistry and new drug manufacturing methods pioneered almost a century ago led to the synthesis of Metformin in 1922 as dimethylbiguanide ( 39). The molecular formula of Metformin is C 4H 11N 5 ( 38). Metformin is hydrophilic and has a molecular weight of 129.16 kDa ( 38). The molecular formula of Metformin HCl, the compound used in clinical preparations, is C 4H 11N 5 Metformin hydrochloride (HCl) is hydrophilic and has a molecular weight of 165.63 kDa ( 37). Metformin is a biguanide derived from a guanidine, galegine, from the French lilac or goat’s rue ( Galega officinalis), which was used for centuries to treat diabetes ( 36). Metformin is the most widely prescribed pharmacotherapeutic agent to treat T2D globally ( 32– 35). This review focuses on the use of Metformin in the management of T2D patients. So far, pharmacotherapies used to treat T2D include metformin, insulin, sodium-glucose cotransporter-2 (SGLT-2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists ( 28– 31). While initial approaches to treatment involved using lifestyle to manage diabetes, it has become clear that this approach needs supplementation with pharmacotherapy to establish and maintain glycemic control ( 27). T2D impacts the children’s longevity and quality of life, and the premature mortality seen in this population is a significant concern ( 26). Microvascular complications manifest as nephropathy, neuropathy, and retinopathy and present much earlier than those in children with type 1 diabetes ( 25). Several conditions are associated with T2D including obesity, dyslipidemia, hypertension, obstructive sleep apnea, polycystic ovary syndrome, and non-alcoholic fatty liver disease ( 20– 24). This rapid deterioration of β-cell function is more rapid in children when compared to adults with T2D ( 15– 19). T2D presents as an aggressive disease with multiple comorbidities, and patients have a progressive failure of β-cell function and progress to insulin dependence within 3-5 years post-diagnosis. The more reproducible test, fasting glucose, is not very practical in children for obvious reasons and does miss those who become hyperglycemic after a carbohydrate challenge.Īs up to 50% of children with T2D are asymptomatic at presentation and are mostly diagnosed when screened because they have obesity, the current prevalence and incidence rates for T2D likely underestimate the true scale of the disease in children ( 9, 14). The use of glycated hemoglobin A1c (HbA1c) has been purposed for monitoring glycemic control in these children rather than establishing the diagnosis alone ( 12, 13). This pattern is coupled with the 30% reproducibility of one of the primary screening tests in children–the oral glucose tolerance test ( 11). There are currently no population-based screening programs for T2D in children the disease remains uncommon in children, with most cases of new-onset diabetes being type 1 diabetes. While initially described as a disease of Indigenous children, current data reveal a surge in T2D across different ethnic groups ( 9, 10). Recent global data suggest incidence rates of up to 31-94 per 100,000 per year and prevalence of up to 160-5,300 per 100,000 in high-risk populations, such as Indigenous and African youth ( 8). Over the past three decades, T2D has increased steadily in children ( 6), with a 7.1% annual increase in incidence rates ( 3) and a 95% increase in prevalence in the USA over almost two decades ( 7). Multiple biosocial drivers contribute to the intertwining of both diseases ( 1, 5). Pediatric type 2 diabetes (T2D) has become a global public health concern driven by childhood obesity ( 1– 4).
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