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Yg Dikutip This Lead To A Decrease PDF
Yg Dikutip This Lead To A Decrease PDF
4: 269-273
DOI 10. 5001/omj.2012.68
Review Article
Abstract Introduction
D
Type 2 diabetes mellitus (DM) is a chronic metabolic disorder in
which prevalence has been increasing steadily all over the world. iabetes mellitus (DM) is probably one of the oldest diseases
As a result of this trend, it is fast becoming an epidemic in some known to man. It was first reported in Egyptian manuscript about
countries of the world with the number of people affected expected 3000 years ago.1 In 1936, the distinction between type 1 and type
to double in the next decade due to increase in ageing population, 2 DM was clearly made.2 Type 2 DM was first described as a
thereby adding to the already existing burden for healthcare component of metabolic syndrome in 1988.3 Type 2 DM (formerly
providers, especially in poorly developed countries. This review is known as non-insulin dependent DM) is the most common form
based on a search of Medline, the Cochrane Database of Systemic of DM characterized by hyperglycemia, insulin resistance, and
Reviews, and citation lists of relevant publications. Subject relative insulin deficiency.4 Type 2 DM results from interaction
heading and key words used include type 2 diabetes mellitus, between genetic, environmental and behavioral risk factors.5,6
prevalence, current diagnosis, and current treatment. Only articles People living with type 2 DM are more vulnerable to various
in English were included. Screening and diagnosis is still based forms of both short- and long‑term complications, which often lead
on World Health Organization (WHO) and American Diabetes to their premature death. This tendency of increased morbidity
Association (ADA) criteria which include both clinical and and mortality is seen in patients with type 2 DM because of the
laboratory parameters. No cure has yet been found for the disease; commonness of this type of DM, its insidious onset and late
however, treatment modalities include lifestyle modifications, recognition, especially in resource-poor developing countries like
treatment of obesity, oral hypoglycemic agents, and insulin Africa.7
sensitizers like metformin, a biguanide that reduces insulin
resistance, is still the recommended first line medication especially Epidemiology
for obese patients. Other effective medications include non- It is estimated that 366 million people had DM in 2011; by 2030
sulfonylurea secretagogues, thiazolidinediones, alpha glucosidase this would have risen to 552 million.8 The number of people with
inhibitors, and insulin. Recent research into the pathophysiology type 2 DM is increasing in every country with 80% of people with
of type 2 DM has led to the introduction of new medications DM living in low- and middle-income countries. DM caused 4.6
like glucagon-like peptide 1 analogoues: dipeptidyl peptidase-IV million deaths in 2011.8 It is estimated that 439 million people
inhibitors, inhibitors of the sodium-glucose cotransporter 2 and would have type 2 DM by the year 2030.9 The incidence of type 2
11ß-hydroxysteroid dehydrogenase 1, insulin-releasing glucokinase DM varies substantially from one geographical region to the other
activators and pancreatic-G-protein-coupled fatty-acid-receptor as a result of environmental and lifestyle risk factors.10
agonists, glucagon-receptor antagonists, metabolic inhibitors of Literature search has shown that there are few data available
hepatic glucose output and quick-release bromocriptine. Inhaled on the prevalence of type 2 DM in Africa as a whole. Studies
insulin was licensed for use in 2006 but has been withdrawn from examining data trends within Africa point to evidence of a
the market because of low patronage. dramatic increase in prevalence in both rural and urban setting,
and affecting both gender equally.11
Keywords: Type 2 diabetes mellitus; Diagnosis; Management; The majority of the DM burden in Africa appears to be type
Newer drugs. 2 DM, with less than 10% of DM cases being type 1 DM.11 A
Abdulfatai B. Olokoba 2011 Centre for Disease Control and Prevention (CDC) report
Division of Gastroenterology, Department of Medicine, estimates that DM affects about 25.8 million people in the US
University of Ilorin Teaching Hospital, Ilorin, Nigeria.
E-mail: drabolokoba@yahoo.com
(7.8% of the population) in 2010 with 90% to 95% of them being
type 2 DM.12
Olusegun A. Obateru It is predicted that the prevalence of DM in adults of which
Department of Medicine, Irrua Specialist Teaching Hospital, Irrua, Nigeria.
type 2 DM is becoming prominent will increase in the next two
Lateefat B. Olokoba decades and much of the increase will occur in developing countries
Department of Ophthalmology, University of Ilorin Teaching Hospital, where the majority of patients are aged between 45 and 64 years.13
Ilorin, Nigeria.
It is projected that the latter will equal or even exceed the former Given inadequate levels of insulin and increased insulin resistance,
in developing nations, thus culminating in a double burden as a hyperglycemia results. The incretins are important gut mediators
result of the current trend of transition from communicable to of insulin release, and in the case of GLP-1, of glucagon suppression.
non-communicable diseases.14 Although GIP activity is impaired in those with type 2 DM, GLP-
1 insulinotropic effects are preserved, and thus GLP‑1 represents
Lifestyle, Genetics, and Medical Conditions a potentially beneficial therapeutic option.30 However, like GIP;
Type 2 DM is due primarily to lifestyle factors and genetics.15 GLP-1 is rapidly inactivated by DPP-IV in vivo.
A number of lifestyle factors are known to be important to the Two therapeutic approaches to this problem have been
development of type 2 DM. These are physical inactivity, sedentary developed: GLP-1 analogues with increased half-lives, and DPP-
lifestyle, cigarette smoking and generous consumption of alcohol.16 IV inhibitors, which prevent the breakdown of endogenous GLP-
Obesity has been found to contribute to approximately 55% of cases 1 as well as GIP.30 Both classes of agents have shown promise,
of type 2 DM.17 The increased rate of childhood obesity between with potential not only to normalize fasting and postprandial
the 1960s and 2000s is believed to have led to the increase in type glucose levels but also to improve beta-cell functioning and mass.
2 DM in children and adolescents.18 Environmental toxins may Studies are ongoing on the role of mitochondrial dysfunction
contribute to the recent increases in the rate of type 2 DM. A weak in the development of insulin resistance and etiology of type 2
positive correlation has been found between the concentration in DM.31 Also very important is adipose tissue, as endocrine organ
the urine of bisphenol A, a constituent of some plastics, and the hypothesis (secretion of various adipocytokines, i.e., leptin, TNF-
incidence of type 2 DM.19 alpha, resistin, and adiponectin implicated in insulin resistance
There is a strong inheritable genetic connection in type 2 DM, and possibly beta-cell dysfunction).30
having relatives (especially first degree) with type 2 DM increases A majority of individuals suffering from type 2 DM are obese,
the risks of developing type 2 DM substantially. Concordance with central visceral adiposity. Therefore, the adipose tissue plays
among monozygotic twins is close to 100%, and about 25% of a crucial role in the pathogenesis of type 2 DM. Although the
those with the disease have a family history of DM.20 Recently, predominant theory used to explain this link is the portal/visceral
genes discovered to be significantly associated with developing hypothesis giving a key role in elevated non-esterified fatty acid
type 2 DM, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, concentrations, two new emerging theories are the ectopic fat
WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX. storage syndrome (deposition of triglycerides in muscle, liver and
KCNJ11 (potassium inwardly rectifying channel, subfamily J, pancreatic cells). These two hypotheses constitute the framework
member 11), encodes the islet ATP-sensitive potassium channel for the study of the interplay between insulin resistance and beta-
Kir6.2, and TCF7L2 (transcription factor 7-like 2) regulates cell dysfunction in type 2 DM as well as between our obesogenic
proglucagon gene expression and thus the production of glucagon- environment and DM risk in the next decade.30
like peptide-1.21 Moreover, obesity (which is an independent risk
factor for type 2 DM) is strongly inherited.22 Monogenic forms Screening and Diagnosis
like Maturity-onset diabetes of the young (MODY), constitutes Tests for screening and diagnosis of DM are readily available. The
up to 5% of cases.23 There are many medical conditions which test recommended for screening is the same as that for making
can potentially give rise to, or exacerbate type 2 DM. These diagnosis, with the result that a positive screen is equivalent to a
include obesity, hypertension, elevated cholesterol (combined diagnosis of pre-diabetes or DM.32 Although about 25% of patients
hyperlipidemia), and with the condition often termed metabolic with type 2 DM already have microvascular complications at the
syndrome (it is also known as Syndrome X, Reaven's syndrome).24 time of diagnosis suggesting that they have had the disease for
Other causes include acromegaly, Cushing's syndrome, more than 5 years at the time of diagnosis.33 It is still based on
thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer, the American Diabetic Association (ADA) guidelines of 1997 or
and drugs.25 Additional factors found to increase the risk of type World Health Organization (WHO) National diabetic group
2 DM include aging,26 high-fat diets, and a less active lifestyle.27 criteria of 2006, which is for a single raised glucose reading with
symptoms (polyuria, polydipsia, polyphagia and weight loss),
Pathophysiology otherwise raised values on two occasions, of either fasting plasma
Type 2 DM is characterized by insulin insensitivity as a result glucose (FPG) ≥7.0 mmol/L (126 mg/dL) or with an oral glucose
of insulin resistance, declining insulin production, and eventual tolerance test (OGTT), two hours after the oral dose a plasma
pancreatic beta-cell failure.28,29 This leads to a decrease in glucose ≥11.1 mmol/L (200 mg/dL).32
glucose transport into the liver, muscle cells, and fat cells. There The 1997 ADA recommendations for diagnosis of DM focus
is an increase in the breakdown of fat with hyperglycemia. The on the FPG, while WHO focuses on the OGTT.32 The glycated
involvement of impaired alpha-cell function has recently been hemoglobin (HbA1c) and fructosamine is also still useful for
recognized in the pathophysiology of type 2 DM.30 determining blood sugar control over time. However, practicing
As a result of this dysfunction, glucagon and hepatic glucose physicians frequently employ other measures in addition to those
levels that rise during fasting are not suppressed with a meal. recommended. In July 2009, the International Expert Committee
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2011. Available at http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. mass index and diabetes mellitus in Asia. A cross sectional pooled analysis of
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2004;127(5):1047-1053 . Curr Opin Endocrinol Diabetes Obes 2011 Apr;18(2):148-152.
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