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\def\citeauthor{~Tholla~Bhagyamma,
              ~Kishore~Bandarapalle,
              ~Dondapati~Tejaswi,
              ~Kammapalli~Ganesh,
              ~Bandi~Haripriya,
              ~Kokkarla~Vyshnavi}
\def\citetitle{\textbf{Review on Diabetes Mellitus Type-2}}
\def\copyrightstmt{This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial- ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.}
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\begin{document}


\def\RunningAuthor{Dondapati Tejaswi et al.}
\firstPage{46}
\articleType{Review Article}
\receivedDate{02 Dec 2022}
\acceptedDate{20 Dec 2022}
\revisedDate{18 Dec 2022}
\journalVolume{3}
\journalIssue{1}
\journalDoi{fjphs.v3i1.339}
\copyrightYear{2023}
\eISSN{2583-116X}
\journalDoi{fjphs.v3i1.339}
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\def\journalTitle{Future Journal of Pharmaceuticals and Health Sciences}

\title{\textbf{Review on Diabetes Mellitus Type-2}}
\author{Tholla~Bhagyamma\textsuperscript{1}\textsuperscript{\href{https://orcid.org/0000-0001-5820-1823}{\XeTeXLinkBox{\includegraphics[height=7pt]{orcid-logo-pharmascope.pdf}}}},  
            Kishore~Bandarapalle\textsuperscript{2}\textsuperscript{\href{https://orcid.org/0000-0003-0032-4331}{\XeTeXLinkBox{\includegraphics[height=7pt]{orcid-logo-pharmascope.pdf}}}},  
            Dondapati~Tejaswi\textsuperscript{*}\textsuperscript{2}\textsuperscript{\href{https://orcid.org/0000-0002-1520-5303}{\XeTeXLinkBox{\includegraphics[height=7pt]{orcid-logo-pharmascope.pdf}}}},  
            Kammapalli~Ganesh\textsuperscript{1}\textsuperscript{\href{https://orcid.org/0000-0001-6976-1594}{\XeTeXLinkBox{\includegraphics[height=7pt]{orcid-logo-pharmascope.pdf}}}},  
            Bandi~Haripriya\textsuperscript{1}, 
            Kokkarla~Vyshnavi\textsuperscript{1}~\\[5pt]{\textsuperscript{1}Department of Pharmacology, Sri Padmavathi School of Pharmacy, Tiruchanoor, Tirupati-517503, Andhra Pradesh, India}~\\{\textsuperscript{2}Department of Pharmaceutics, Sri Padmavathi School of Pharmacy, Tiruchanoor, Tirupati-517503, Andhra Pradesh, India}}

\begin{abstract}
Type 2 diabetes mellitus is a metabolic disorder that is becoming more and more common everywhere in Diabetes mellitus. Due to an ageing population, it was anticipated that the number of impacted persons will triple in the following ten years, placing further strain on healthcare professionals, especially in developing nations. In many nations around the world, this tendency is quickly spreading like an epidemic. The World Health Organization (WHO) and American Diabetes Association (ADA) protocols, which take into account clinical and laboratory factors, continue to serve as the basis for diagnosis and screening. Attempting to alter one's way of life, managing obesity, using oral antihyperglycemic drugs, as well as using insulin additives like metformin, a biguanide which reduces insulin resistance and is still the medicine of choice, are all recommended. Alpha-glucosidase inhibitors, insulin, phenothiazines, or non-sulfonylurea secretagogues are additional effective medications. Recent research into the pathophysiology of type 2 diabetes has resulted in the development of novel medications, including glucagon-like peptide one analogous drugs, dipeptidyl peptidase-IV inhibitors, sodium-glucose cotransporter two and 11{\ss}-hydroxysteroid dehydrogenase 1 inhibitors, insulin-releasing glucokinase activators, and pancreatic-G-protein-coupled fatty acid-receptor inhibitors agonist, despite having a license to use it since 2006, inhaled insulin has been taken off the market due to little demand.
\end{abstract}\def\keywordstitle{Keywords}

\begin{keywords}Diabetes Mellitus Type 2,\newline Diagnosis,\newline Treatment,\newline Newer Medications
\end{keywords}
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\makeatletter{\raggedright{\Large$^\ast$}Corresponding Author\par Name:\ Dondapati~Tejaswi~\\ Phone:\ 8688941902~\\  Email:\ tejadondapati2002@gmail.com
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\section{Introduction}
Diabetes mellitus may be one of the oldest illnesses that humans have ever encountered (DM). It was initially mentioned in Egyptian literature some 3000 years ago \unskip~\cite{1618438:26634394}. The metabolic syndrome was first recognized to include type 2 diabetes in 1988 \unskip~\cite{1618438:26634399}. The most prevalent kind of diabetes, type 2, is characterised by hyperglycemia, insulin sensitivity, as well as generally insufficient insulin secretion \unskip~\cite{1618438:26634400}. Non-insulin-dependent diabetes was the original name for type 2 diabetes. Long-term and short-term problems are more common in people with type 2 DM, many of which result in early death. Patients with type 2 diabetes often experience greater rates of morbidity and mortality since the disorder is so common, has a stealthy beginning, and takes a while to diagnose, especially in poorer nations with limited resources like Africa \unskip~\cite{1618438:26634398}.

\textbf{Epidemiology}

There are notable regional variations in the prevalence of type 2 diabetes \unskip~\cite{1618438:26634396}, influenced by environmental and behavioral risk factors. It is anticipated that the prevalence of adult-onset diabetes{\textemdash}of which type 2 DM is becoming more common{\textemdash}will increase during the next 20 years. The bulk of patients in emerging nations, where this increase will be most significant, are between the ages of 45 and 64 \unskip~\cite{1618438:26634387}. Projections indicate that as infectious diseases give way to non-communicable conditions, the latter will eventually equal or perhaps surpass the former in rising nations, resulting in a double burden \unskip~\cite{1618438:26634385}.

\textbf{Lifestyle, Genetics, and Medical Conditions}

Type 2 DM is caused mainly to lifestyle factors and genetics \unskip~\cite{1618438:26634397}. The start of type 2 DM is known to be significantly influenced by various lifestyle variables. These include excessive alcohol use, smoking, sedentary behavior, and lack of physical activity. It has been discovered that obesity has a role in about 55\% of type 2 DM cases. The number of children and adolescents are likely to have increased due to the growth in juvenile obesity between the 1960s and 2000s. There has been evidence of a weakly positive correlation between the prevalence of type 2 DM and the amount of bisphenol A, a component of certain plastics, in urine \unskip~\cite{1618438:26634391}. The current rise in type 2 DM prevalence could be partial attributed to environmental toxins.

Type 2 diabetes is genetically significantly heritable, and the likelihood of contracting the condition is markedly increased by having first-degree relatives who already have it. Monozygotic twin concordance is about 100\%, and roughly 25\% of people with the disease have a family history of diabetes mellitus. A substantial relationship between type 2 diabetes and several Recently identified genes include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX. The islet ATP-sensitive potassium channel KCNJ11 and TCF7L2 encode proglucagon gene expression and glucagon-like peptide-1 synthesis, respectively. Kir6.2 (key transcription 7-like 2) regulates proglucagon expression of genes. In addition, obesity is a risk factor for diabetes type 2 and has a strong genetic component. Monogenic instances represent up to 5\% of all cases, including Sophistication Hyperglycemia of a Juvenile (MODY). Numerous medical problems have the potential to cause or worsen type 2 DM. These include excess weight, high blood pressure, raised cholesterol (combined hyperlipidemia), and Reaven's syndrome, a disorder also referred to as metabolic syndrome or Syndrome X.

Additional causes include amyloidosis, Cushing's disease, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, malignancy, and medicines. A less active lifestyle, high-fat diets, and aging have increased the prevalence of type 2 DM \unskip~\cite{1618438:26634395}.

\textbf{Pathophysiology}

Insulin sensitivity is a hallmark of type 2 diabetes and is brought on by glucose intolerance, decreased insulin production, as well as finally malfunctioning pancreatic beta cells. Both classes of medications have shown promise, improving beta-cell mass and function and regulating fasting and postprandial glucose levels. Research is still ongoing to determine the importance of neurodegeneration in genesis of diabetes type 2 as well as the development of insulin resistance \unskip~\cite{1618438:26634376}. 

\textbf{Screening and Diagnosis }

There are many readily available tests for DM diagnosis and screening. A positive screen is equivalent to a pre-diabetes or DM diagnosis because the test recommended for both screening and diagnosis is the same. And although 25 percent of type 2 DM patients already had microvascular issues at the time of diagnosis, meaning they had the illness for more than five years at that point \unskip~\cite{1618438:26634374}, they were nonetheless diagnosed with it. It continues to be based on the American Diabetes Association (ADA) recommendations from 1997 or the National Diabetic Group criteria from the World Health Organization (WHO), They are really for two high values at two separate occasions, either one of fasting blood glucose (FPG) 37.0 mmol/L (126 mg/dL) or an oral glycemia. These refer to singular increased glycemic readings with symptoms (polyuria, polydipsia, polyphagia, and weight loss) \unskip~\cite{1618438:26634381}.

The WHO emphasizes just on Oral glucose tolerance test, while the 1997 ADA guidelines for the diagnosis for DM place more emphasis upon that FPG. When analyzing blood sugar management throughout time, fructosamine as well as fasting plasma glucose haemoglobin (HbA1c) were always useful. However, in addition to the suggested procedures, real doctors frequently take further actions. The International Expert Committee (IEC) proposed the addition of the HbA1c value of 36.5\% for DM as an additional diagnostic criterion in July 2009. This group recommended that the term "pre-diabetes" be phased out, but it also selected the HbA1c range of 36.0\% to 6.5\% to identify people at high risk of developing DM \unskip~\cite{1618438:26634383}.

There is no clear HbA1c cutoff point that marks the beginning of DM and the end of normalcy, similar to glucose-based testing. The IEC decided to propose a diagnostic cutoff for DM that emphasizes specificity, noting that this struck a balance between the stigma and cost of incorrectly classifying people as having diabetes and the minor clinical repercussions of postponing the diagnosis in a patient with an HbA1c level under 6.5\%.

\textbf{Management}

By dietary and lifestyle changes. According to studies, sustaining the body weight index around 25 kg/m2, following a diet fiber - rich or essential fats whilst consuming a low amount in saturated as well as trans fats, while exercising on a regular basis are all advantageous. Modest consumption of alcohol substantially reduces the risk of type 2 DM \unskip~\cite{1618438:26634377}. Suggesting that changing one's lifestyle can prevent the bulk of class 2 DM. A medical nutrition assessment should be given to type 2 diabetic patients, and lifestyle advice should be customized for each patient's physical and functional capabilities.

\textbf{Pharmacological Agents}

\textbf{Biguanides}

In patients who are overweight or obese, biguanides{\textemdash}of which metformin is the most frequently prescribed{\textemdash}suppress GLUT-enhancer component was activated for an accelerate uptake of glucose, impaired insulin generation, insulin levels, oxidation of fatty acids as well as reduce gastrointestinal glucose absorption \unskip~\cite{1618438:26634384}. An additional mechanism of action for metformin, according to research released in 2008, is the stimulation of AMP-activated protein kinase, an enzyme involved in the production of hepatic gluconeogenic genes. Compared to sulfonylureas, it has a reduced incidence of hypoglycemia. Metformin should be used with caution in senior diabetics with renal impairment due to the risk of developing lactic acidosis. 

\textbf{Sulfonylureas}

These are often well absorbed yet associated with such a possibility of hypoglycemia when these stimulate spontaneous insulin production. Elderly DM persons consuming sulfonylureas have such a 36\% increased hypoglycemia risk when compared to younger patients. 

Contrary to glipizide, gluburide has linked to higher rates in hyperglycemia. consumption of alcohol, ages above 60, use of insulin or other insulin sensitizers consecutively, subsequent hospital discharged\textbf{\space }misuse, calorie restriction, multiple drugs, or medications that increase the effects of sulfonylureas are some risk factors for hypoglycemia \unskip~\cite{1618438:26634380}. Short-acting glipizide is advised in older patients with DM rather than long-acting sulfonylureas like glyburide.

\textbf{Meglitinides}

Although the binding location is different, Repaglinide as well as Nateglinide are non-sulfonylurea secretagogues which stimulate insulin released through pancreatic beta cells through operating just on ATP-dependent K-channel. Meglitinides have such a quick start as well as a shorter time half-life (4-6 hrs.), which reduces the risk of hypoglycemia. Meglitinides are administered before meals to control postprandial blood glucose. Pre-prandial administration gives you flexibility if you miss a meal without increasing your risk of hypoglycemia \unskip~\cite{1618438:26634378}. Except for those with end-stage renal illness, patients with renal insufficiency do not require dose adjustment because repaglinide is mainly processed in the liver and excreted in tiny amounts through the kidneys. 

\textbf{Thiazolidinediones}

Thiazolidinedione is an insulin sensitizer and a specific ligand for the transcription factor peroxisome proliferator-activated gamma.\textbf{\space }They are the first medications to treat type 2 DM patients' fundamental issue of insulin resistance \unskip~\cite{1618438:26634392}. This class now mainly consists of pioglitazone following the Food and Drug Administration's (FDA) recent recommendation to restrict the use of rosiglitazone due to an increase in cardiovascular events associated with rosiglitazone \unskip~\cite{1618438:26634393}. Pioglitazone is well tolerated and can be used in cases of renal impairment by older persons because it is not linked to hypoglycemia. However, its usage may be restricted in older people with DM because of worries about peripheral edema, fluid retention, and fracture risk in women. Pioglitazone is contraindicated in people with class III-IV heart failure and should be avoided in elderly adults with congestive heart failure.

\textbf{Alpha-Glucosidase Inhibitors}

Although not frequently used to treat type 2 DM patients, acarbose, voglibose, and miglitol are probably safe and effective. These medications should not be used in patients with severe renal impairment because they are most helpful in treating postprandial hyperglycemia. Due to the high rates of side effects such as diarrhea and flatulence, their use is typically restricted \unskip~\cite{1618438:26634388}. A study found that voglibose's newest medication considerably improved glucose tolerance to delay disease progression.

\textbf{Incretin-Based Therapies}

They can be used alone, in conjunction with exercise and diet, or combination with hypoglycemic medications in individuals with type 2 diabetes. Examples include Liraglutide and the incretin mimic Exenatide \unskip~\cite{1618438:26634386}.

\textbf{Dipeptidyl-Peptidase IV Inhibitors}

DPP IV inhibitors block DPP-4, a common enzyme that permanently disables GLP-1 or GIP. Raising the hormones' levels in the body help improve type 2 diabetes islet function and glycemic management. It is currently unclear how long-lasting the effect will be on beta-cell morphology, process, and glycemic control. A novel family of anti-diabetic medications known as DPP-4 inhibitors is just as efficient as existing medications. They work well as add-on therapy combined with metformin, thiazolidinediones, and insulin and as monotherapy in individuals with inadequate diet and exercise management. DPP-4 inhibitors are safe, have a low risk of hypoglycemia, and have no effect on weight. However, they are rather pricey \unskip~\cite{1618438:26634389}.

\textbf{Insulin}

Aside from other oral hypoglycemic medications, insulin can be utilized. Basal insulin augmentation therapy is advantageous if some beta cell activity is still present. In the event of beta cell fatigue, basal-bolus insulin must be changed. Rescue therapy with In cases of hypoglycemia overdose, replenishment was required and therefore should mimic the pancreatic beta cells' regular insulin production \unskip~\cite{1618438:26634375}. A 4 kinds of insulin which are injected intravenously were rapid-acting, short-acting, intermediate-acting, or long-acting. Comparing to short-acting counterparts, lengthy ones are much less likely to result in hyperglycemia.

\textbf{Insulin Analogs}

The ability of insulin therapy to match typical physiologic insulin production was not very good. NPH insulin, Lente insulin, and ultra-Lente insulin are traditional intermediate- and long-acting insulins. These insulins have irregular absorption and activity peaks that can result in hypoglycemia. The novel insulin analogs' onset and durations of action range from rapid to protracted, and their pharmacokinetic profiles are distinct from those of regular insulins. Currently, insulin lispro and insulin as part are two rapid-acting insulin analogs, and insulin glargine is one long-acting insulin analog \unskip~\cite{1618438:26634401}.

\textbf{Future in Drug Therapy Inhaled Insulin} \textbf{\space }

Rapidly acting insulin inhaled for treating type 1 and type 2 diabetes in humans was made accessible in 2006 after receiving approval from the European Medicines Evaluation Agency and the Food and Drug Administration \unskip~\cite{1618438:26634379}.

\textbf{Others}

Inhibitors like sodium-glucose cotransporter 2, they enhance renal glucose, also inhibitor of 11{\ss}-hydroxysteroid dehydrogenase 1, which reduces the impact of glucocorticoids just on hepatic as well as fats clearance. For the creation of new diabetic medications, research is being done on insulin-releasing Glucagon receptors antagonist, phosphorylase stimulators, pancreatic-G-protein-coupled fats receptors agonist, as well as metabolism inhibitor of hepatic glucose production \unskip~\cite{1618438:26634382}. 
    
\section{Conclusion}
Type 2 diabetes is such a metabolic condition that can be prevented by making lifestyle changes, controlling your diet, and controlling your weight. Despite improvements in drug research and a new understanding of the pathophysiology of the illness, a cure is still not in sight. Education of the populace is still essential for containing this new disease. People with type 2 diabetes should receive management designed to enhance their quality of life.
    
\section{Acknowledgement}
The corresponding author desires to explict utmost gratitude to the Management and Prof. Dr. D. Ranganayakulu, M. Pharm., Ph. D., Principal, Sri padmavathi school of pharmacy, Tiruchanoor, Andhra Pradesh, India, for presenting all the necessary laboratory demands of the research and constant.

\textbf{Funding Support}

The authors declare that they have no funding support for this study.

\textbf{Conflict of Interest}

The authors declare that there is no conflict of interest.
    

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