CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 3, May/June 2011
AFRICA
149
Adiponectin is copiously secreted from mature adipocytes,
38-40
with expression negatively correlating with body mass index
(BMI).
41,42
Consequently, lean subjects have high levels, whereas
obese subjects have low plasma levels. Decreased expres-
sion of adiponectin is observed in a number of obesity-relat-
ed co-morbidities such as type 2 diabetes,
43,44
the metabolic
syndrome,
45,46
non-alcoholic steatohepatitis
16
and CAD.
47,48
It has
also been found that the protein is anti-diabetic, increasing
insulin sensitivity, glucose uptake and fat oxidation, as well as
suppressing hepatic glucose output.
49-51
The protein may also alter
basal insulin secretion
52
and modulate satiety, increasing food
intake and suppressing energy expenditure when fasting, but
surprisingly having opposite effects after refeeding.
53
It is also
anti-atherogenic
47,54
and anti-inflammatory.
55
Whereas adiponectin decreases during obesity, there are other
glucose-lowering adipokines that correlate positively with BMI.
Circulating apelin increases in obesity
56
and has been show to
lower glucose in normal and obese mice.
57
Homozygous apelin
knockout mice have severe heart failure in response to pres-
sure overload and diminished heart contractility in aged mice,
58
indicating a role for the adipokine in maintaining cardiac func-
tion. Visfatin is an adipokine that is predominantly expressed
in visceral adipose tissue and has been attributed to having
insulin-like properties,
59
although this has since been disputed,
60,61
and recently visfatin has been shown to have pro-inflammatory
effects.
62
Vaspin is a serine protease inhibitor and is reported to
reduce expression of leptin, resistin and TNF
α
and improves
insulin sensitivity.
63,64
The recently discovered adipokine chemerin
65,66
increases
insulin sensitivity in 3T3-L1 adipocytes
67
and is essential for
normal adipocyte differentiation.
65,66,68
However, it has also been
shown to lower glucose tolerance in murine models of obesity/
diabetes
69
and to cause insulin resistance in human skeletal
muscle cells, where it was also observed to be pro-inflamma-
tory.
70
Consequently adipose tissue secretes both pro- and
anti-inflammatory cytokines which modulate metabolism by
altering insulin resistance. Generally, pro-inflammatory cytokine
production increases and anti-inflammatory expression decreas-
es during insulin resistance and obesity.
Obesity and cardiovascular disease in Africa
Studies have shown that the prevalence of both cardiovascular
disease (CVD)
71
and obesity
7
is rising in Africa. Although it is
not certain that these two findings are linked, the observation that
CVD is more common in obese Africans
72
supports this premise.
This recent rise in the prevalence of obesity in Africa is attributed
to increased urbanisation and the associated ease of access to a
more westernised, calorie-dense diet.
73
Within Africa, the prevalence of CVD and its risk factors
differs across the various resident population groups.Accordingly,
mortality due to heart disease is higher in the Asian-Indian and
European ethnic groups of South Africa when compared to the
indigenous black African population.
74
Fasting serum cholesterol
and triglyceride levels are higher in Asian-Indian than African
subjects,
75
with type 2 diabetes being more prevalent in the
former population group.
76
The reasons for these ethnic differ-
ences in disease prevalence rates and cardiovascular risk factors
are not fully understood, although it has been suggested that
the higher abdominal fat mass observed in Asian-Indian and
European compared to African subjects may be involved.
77
It is, however, of note that African subjects tend to be more
insulin resistant than Europeans
78,79
even though they have less
visceral adiposity. This would suggest either that visceral fat
in African compared to European subjects has a greater abil-
ity to reduce insulin sensitivity, or that visceral adiposity is not
involved in determining the level of whole-body insulin sensitiv-
ity in the African population. The latter hypothesis is unlikely
since it has been shown that waist circumference, independently
of BMI, is a determinant of insulin sensitivity in this popula-
tion group.
80
It is also possible that subcutaneous abdominal fat
may play a more prominent role in determining whole-body
insulin sensitivity in African than European females, as has been
observed in a previous study.
79
Previous investigators have suggested that obesity in African
subjects is benign. This hypothesis was based on reports that
blood pressure, glucose and lipid levels were not elevated
in obese compared to lean African females.
81
However, this
hypothesis is challenged by data showing that there is a higher
prevalence of CVD in obese compared to non-obese African
subjects.
72
Furthermore, it must be noted that these studies
81
did
not take into account body fat distribution, which is a major
contributing factor to the pathogenesis of obesity-related disor-
ders. It is also of interest to note that the African countries with
the highest prevalence of obesity have the highest prevalence of
obesity-related disorders, such as type 2 diabetes.
82
Adiposity and insulin resistance as a
biological advantage
Obesity has many negative connotations with regard to health.
It is associated with an increased risk of many diseases, rang-
ing from asthma to cancer. However, body fat does have an
important physiological role, including the maintenance of body
temperature and triglyceride storage. It also acts as an endocrine
modulator of insulin sensitivity and appetite. The negative effects
of adiposity on insulin sensitivity are often viewed as purely
pathological. However, insulin resistance has been proposed to
have an important biological role. It is now thought that insulin
resistance is a normal physiological response to obesity to slow
down triglyceride deposition in adipose tissue.
83
Studies have
indeed shown that insulin resistance may protect against weight
gain.
84,85
Furthermore, the biological adaptation of insulin resist-
ance has been proposed as advantageous in prehistory, during
times of feast and famine. The ability to readily store energy
as fat would be beneficial until excessive adiposity would limit
the capability of our ancestors to hunt and escape predation.
Thus, insulin resistance would act to limit the rate of fat deposi-
tion. It is therefore possible that insulin resistance evolved to
limit fat deposition in a period of human evolutionary history
when excessive caloric intake was not a common occurrence.
In modern times however, access to calorie-dense foods is not
limited and this homeostatic mechanism for limiting excessive
weight gain has been overpowered by new environmental condi-
tions in which famine has been replaced by feast.
Adipose tissue may play an important role in modulating
immunity. Adipocytes secrete a wide range of different cytokines
that have both pro- and anti-inflammatory properties. Also,
lymph nodes are normally found within adipose tissue depots
and studies have demonstrated a strong interrelationship between
these two tissue types. Therefore, the cells of the lymph node are
