Delaware County Medical Society Summer/Fall 2020 - 29

FEATURE

Obesity, A Metabolic Disorder
with Clinically Significant Co-Morbidities
A Review
By Donald Powers, MD

O

besity is defined as a body mass (BMI) 30
kg per m. On first assessment one may
note body size. However, one should first
clinically assess for the presence of any
co-morbidities associated with obesity; viz., diabetes,
dyslipidemia, non-alcoholic fatty liver, or what is
described by Abel (2010) as lipotoxic cardiomyopathy.
It is estimated approximately one-third of obese
individuals are defined as metabolically healthy, with no
obesity-associated health problems other than adverse
consequencies associated with weight gain (Sears and
Perry 2015). However, two-thirds of obese individuals do
have such obesity-associated co-morbidities. What can
be the explanation for why some obese individuals remain
metabolically healthy and others do not? The explanation
may lie in how one's body processes fat metabolism.
In those obese individuals with obese-associated comorbidities there is evidence of a fundamental mismatch,
an imbalance, present between the quantity of lipid to be
metabolically oxidized and the capacity of an organ in the
body to complete the oxidative process; both in the betaoxidative pathway for fatty acid metabolism, a stepwise
degradation in size of long-chain fatty acid to a two carbon
molecule - so as to enter a mitochondria, an organelle
where the oxidation process is completed in its tricarboxlic
(Krebs) cycle; and the capacity of the mitochondria
themselves in an organ for oxidative completion (Erion and
Schulman 2010).

This mismatch between the quantity of lipid for its
metabolic oxidative disposal (the "supply") and a body
organ's capacity to complete the oxidative process in
its mitochondria results in the formation of fatty acid
intermediate metabolites, as DAG (diacylglycerol), a
bio-active signally compound. As DAG accumulates in
the tissues of an organ; such as insulin-action responsive
organs as skeletal muscle and liver, the intracellular
accumulation of DAG, which has the ability to disrupt the
insulin signaling cascade (refer to Figure One); results in
the onset of insulin resistance, and in the failure of insulin
action to regulate the orderly metabolic functions operating
in health within these organs.
Erion and Schulman list in their report the etiologic
metabolic causes where such a lipid metabolic mismatch
arises. These are (1) excessive caloric intake, (2) a defect
in the adipocyte function (the cell in adipose tissue that is
metabolically), (3) uninhibited lipolysis (release of a large
quantity of fatty acid into the circulation from insulinresistant adipose tissue, and (4) defects in mitochondria
themselves for oxidative function and gene variation.
Metabolic imbalance due to the quantity of lipid for
oxidative disposal (the "supply side" of the imbalance);
such an imbalance can easily be attributed to an excessive
caloric intake in obesity, but an increased quantity of fatty
acid in the circulation also arises with the onset of insulin
resistance in the adipocyte, cells in adipose tissue that are
metabolically active. In these cells is where triglyceride
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Delaware County Medical Society Summer/Fall 2020

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