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DIABETES AND
OBESITY

DIABETES & OBESITY:

How are they related and how we can prevent them.

By Sherryl D. Mitchell Hernandez, MD

A ll of us love food. We love how it tastes and how it makes

us feel after we eat! Plus, we live in a city with a great culi-
nary background. but we must take into consideration
that if we do not take the necessary measures to either control the
amount and what we eat, we will be at a great risk of obesity and,
therefore, diabetes.
Most patients with type 2 diabetes are obese and there has been
a dramatic increase in the incidence and prevalence of type 2 dia-
betes over the past 20 years. Currently, over a third (34 percent) of
U.S. adults are obese (defined as bMI >30 kg/m2), and over 11 per-
cent of people aged ≥20 years have diabetes.
Excess weight is an established risk factor for type 2 diabetes. Re-
cent studies have identified “links” between obesity and type 2 dia-
betes involving proinflammatory cells, insulin resistance, deranged
fatty acid metabolism, and cellular processes such as mitochondrial
dysfunction, which is where our energy is produced. The influence
of obesity on type 2 diabetes risk is determined not only by the de-
gree of obesity but also by where fat accumulates. Increased upper
body fat includes visceral adiposity, as reflected in increased abdom-
inal girth or waist-to-hip ratio, which is associated with the metabolic
syndrome, type 2 diabetes, and cardiovascular disease. The link be-
tween obesity and hyperinsulinemia, first identified about 50 years
ago, reflects compensation by insulin-secreting β-cells to systemic
insulin resistance. Although mechanisms underlying this coupling
(e.g., mild hyperglycemia and raised levels of circulating free fatty
acids) remain elusive, obese normoglycemic individuals have both
increased β-cell mass and function. Obesity-induced glucose intol-
erance reflects failure to mount one or more of these compensatory
responses. The Genome-wide association scans (GWAS) and can-
didate gene approaches now have identified ∼40 genes associated
with type 2 diabetes and a similar number, albeit largely different,
with obesity. Most type 2 diabetes genes appear to be related to β-
cell dysfunction, with many fewer involved in pathways related to
insulin resistance independent of obesity. Although numerous dia-
betes- and obesity-associated genes have been identified, the known

16 San Antonio Medicine • December 2018