The Relationship Between Obesity and Type 2 Diabetes Mellitus

Obesity and type 2 diabetes 1
THE RELATIONSHIP BETWEEN OBESITY AND TYPE 2 DIABETES MELLITUS
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Obesity and type 2 diabetes 2
Abstract
Diabetes and insulin resistance are strongly correlated to body mass index. For individuals who
are obese, the quantity of glycerol, proinflammatory markers, nonesterified fatty acids, and
cytokines among other elements that play a role in the advancement of resistance to insulin is
augmented. Impairment of the pancreatic Beta islet cells and thus causing improper control of
the blood sugar form the foundation of diabetes pathogenesis. Type 2 diabetes mellitus
progression is accelerated when insulin resistance accompanies impairment of the pancreatic
Beta islet cells. It is therefore undoubtable that high body mass index and progressive weight
gain are key contributors to the rising occurrence of type 2 diabetes. In this report, therefore,
comprehensive inscription of the interrelation between dysfunction of pancreatic β-cell and
insulin resistance with obesity is made.

Obesity and type 2 diabetes 3
1.0 Introduction
Diabetes mellitus is a long term disorder with the potential of altering the metabolism of fats,
proteins and carbohydrates. It is primarily caused by low secretion of insulin due to either
marked or advanced incapability of the pancreatic β-Langerhans islet cells to yield insulin. It can
also be caused by defective uptake of insulin in the outlying flesh. There are two broad
classifications of diabetes which are; type 1 diabetes mellitus and type 2 diabetes mellitus.
The etiology and pathophysiology of type 2 diabetes are relatively different in comparison to that
of type 1 diabetes. Type 2 diabetes is the utmost established and is commonly characterized by
either production of insulin in low amounts from the pancreatic Beta cells or resistance of insulin
in the peripheral tissue (Sheehan & Ulchaker, 2011). When resistance to insulin occurs, the level
of plasmic fatty acids elevates subsequently lowering transport of glucose into the muscle cells
and elevatin itemization of fats. Consequently, hepatic glucose production raises. Development
of type II diabetes requires the simultaneous occurrence of pancreatic Beta-cell dysfunction and
insulin resistance must prevail. Being obese emanates from some kind of insulin resistance and
thus plays a significant role in the progression of type 2 diabetes.
In Australia, type 2 diabetes is a menace that is negatively impacting the lives of people. The
disease was traditionally associated with the elderly people but the trend is currently changing
(Ahmad, 2013). Recent reports indicate that with the ever-changing lifestyle, the incidence of
type 2 diabetes is increasing even to the younger generation. This report will therefore
comprehensively discuss how obesity plays part in promoting type 2 diabetes among individuals
aged 30-50 years. It will commence with a discussion of obesity-related factors that accelerate
the threat of acquiring type 2 diabetes. This section will adopt relevant literature and bring into
the limelight insulin resistance mechanisms associated to obesity, progressive β-cell dysfunction

Obesity and type 2 diabetes 4
mechanisms in obese persons, genetic aspects associating obesity to diabetes and the possibility
of shared pathogenesis between obesity and type 2 diabetes mellitus. It will conclude with
recommendations that could be implemented to curb the menace in Australia.
2.1 Means through which obesity promotes type 2 diabetes among people aged 30-50 years.
2.1.1 Insulin resistance mechanisms associated with obesity
Type 2 diabetes is not only influenced by obesity through the degree of resistance to insulin but
also by the body part where fat amasses. Accumulation of fat in the upper body such as visceral
adiposity, which manifests itself through increased weight to hip ratio or abdominal girth is
directly concomitant to cardiovascular disease, metabolic disorder and more so, type 2 diabetes.
Other than differences in the distribution of the body fat, upcoming evidence put it forward that
glucose homeostasis is affected differently by adipose tissue of different subtypes which function
distinctly (Chadt, et al., 2018). Adults, including those in the category of 30-50 years, have
variable and limited numbers of brown fat cells. These cells are largely involved in
thermogenesis in addition to having the potential of influencing the expenditure of energy and
susceptibility to obesity.
There are three distinct and key modes of action that have been suggested to interconnect obesity
and insulin resistance and consequently predisposing obese persons to type 2 diabetes. The first
mechanism involves increased production of cytokines or adipokines. They include the retinol
binding protein 4, resistin and the tumor necrosis factor-α. All the aforementioned have been
proved to contribute to lowered levels of adiponectin production as well as raising the resistance
of the body to insulin. The second mechanism centers on the deposition of ectopic fat (Al-
Goblan, et al., 2014). The body parts that are particularly affected by this deposition are the
dysmetabolic sequelae, skeletal muscle and more importantly in the liver. The last mechanism is