Diabetes Mellitus

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 Diabetes Mellitus
>>> Diabetes mellitus (DM) describes a group of chronic metabolic disorders.
DM is characterized by hyperglycemia that may result in long-term
microvascular and neuropathic complications.

These complications contribute to DM being the leading cause of:

 New cases of blindness among adults
 End-stage renal disease
 Nontraumatic lower limb amputations

Macrovascular complications (coronary artery disease, peripheral vascular

disease, and stroke) are also associated with DM.

DM is characterized by a complete lack of insulin, a relative lack of insulin, or

insulin resistance as well as disorders of other hormones. These defects result
in an inability to use glucose for energy.
Diabetes Mellitus
 Diabetes Mellitus
The increasing prevalence of DM is partly caused by three influences:
 Lifestyle
 Ethnicity
 Age
 Diabetes Mellitus
 Lifestyle
A sedentary lifestyle coupled with greater consumption of high-fat, high-
carbohydrate foods, and larger portion sizes have resulted in increasing rates of
obesity.

Current estimates indicate that 36.5% of the US population is obese when

obesity is defined as a body mass index (BMI) of greater than 30 kg/m2.

Only 1 in 5 adults currently meet physical activity guidelines set forth by the
Centers for Disease Control and Prevention (CDC) and persons living in the
American South are less likely to be physically active than those living in other
areas of the country.
 Diabetes Mellitus
 Ethnicity
Certain ethnic groups are at a disproportionately high risk for developing type 2
DM (T2DM). The prevalence of DM is 15.1% among American Indians/Alaska
Natives, 12.7% among non-Hispanic blacks, and 12.1% among persons of
Hispanic ethnicity; whereas, among non-Hispanic whites, the prevalence is only
7.4%.

Socioeconomic status, when examined as a function of education level, also

plays a role in the development of DM. The rate of DM is 12.6% for persons with
less than a high school education versus 7.2% for those with education beyond
high school.
 Diabetes Mellitus
 Age
As the population ages, the incidence of T2DM is expected to increase. Type 1
DM (T1DM) is usually diagnosed before age 30 years but can develop at any
age.

As a result, patients over 30 years of age who newly develop T1DM may be
misdiagnosed as having T2DM. Autoimmune destruction of the β-cells causes
insulin deficiency. T2DM accounts for approximately 90% to 95% of all
diagnosed cases of DM, is progressive in its development, and is often
preceded by an increased risk for diabetes (previously known as prediabetes).
A combination of insulin deficiency, insulin resistance, and other hormonal
irregularities, primarily involving glucagon, are key problems with T2DM.

The majority of people with T2DM are overweight, and an increasing number
of cases in children have been observed.
Diabetes Mellitus
Diabetes Mellitus
 Epidemiology and Etiology
In the U.S.,
34.2 million Americans—just over 1 in 10—have diabetes.
88 million American adults—approximately 1 in 3—have prediabetes

422 million people worldwide have diabetes, particularly in low-and middle-

income countries (WHO)

Did you know?

Diabetes is one of the leading causes of death in the world

2 main types
Type 1 diabetes (lack of insulin) and type 2 diabetes (ineffective use of insulin).
Epidemiology and Etiology
Types of DM
 Epidemiology

https://diabetesatlas.org/data/en/world/ https://diabetesatlas.org/data/en/
Epidemiology and Etiology
Pathophysiology and drug targets:
T2D is a heterogeneous disorder with a complex pathophysiology, in which genetic and environmental
factors contribute to dysfunction of various organ systems that control glucose homeostasis.

Insulin resistance of liver, adipose, and skeletal muscle tissue results in respectively impaired insulin-
induced reduction of HGP, lipolysis, and impaired insulin-stimulated glucose uptake.

Hyperglycemia evolves when pancreatic β-cells are unable to secrete sufficient insulin to overcome
insulin resistance (i.e., β-cell failure). In addition, α-cell dysfunction, characterized by fasting and
postprandial hyperglucagonemia, stimulates HGP, which further augments hyperglycemia.

Moreover, the efficacy of gut-derived incretin hormones GLP-1 and GIP to facilitate meal-related insulin
release and glucagon suppression is impaired. The kidneys contribute to hyperglycemia by increasing
tubular glucose reabsorption, presumably through upregulation of SGLT2 and increased renal
gluconeogenesis. Last, in the development of T2D, impaired activation of satiety centers in the brain
stimulates excessive food intake, and insulin resistance in the brain may alter central control of
metabolic homeostasis. Pleiotropic drug effects are illustrated by the frame and color of the boxes.
Green indicates body weight loss, blue indicates body weight neutrality, and red indicates body weight
gain.
A dotted frame indicates blood pressure reduction, and a solid frame indicates blood pressure
neutrality. SU, sulfonylurea; TZD, thiazolidinedione.