Cardiovascular Journal of Africa: Vol 22 No 3 (May/June 2011) - page 41

CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 3, May/June 2011
AFRICA
151
BMI-matched Europids, and yet are more insulin resistant.
77-79
The use of high-throughput gene-screening technology, which
has yielded important information on the polygenic nature of
obesity via genome-wide association studies
132
should therefore
be used in African populations to determine the genetic input
to adiposity and body fat distribution. It is possible that ethnic
differences in insulin sensitivity and the prevalence of obesity-
related disorders are due to differences in the secretory output
of adipocytes. The comparison of adipocyte secretomes across
population groups using the new technologies developed for
the analysis of complex mixtures of bioactive molecules
133
may
therefore be very worthwhile.
The future of the use of adipose-derived stromal cells
(ADSCs) for the treatment of human disease looks very promis-
ing. Such cells have already been used to correct cranial defects
in humans,
119
and preliminary studies in man to rectify cardio-
vascular
134,135
and soft tissue
136-138
defects hold hope for the future
use of ADSCs in the treatment of muscle and cartilage defects
and heart infarcts. However, before this becomes a reality, there
are a number of technical problems that need to be overcome.
The methods used for the large-scale isolation of ADSCs and
their efficient conversion into the correct cell phenotype must be
improved and standardised. Also, the long-term safety of the use
of these cells in humans must be explored, initially by the devel-
opment of the appropriate animal models. Stem-cell therapy is
already available for the treatment of haematological malignan-
cies in specialised medical centres within Africa
139
and therefore
it is feasible that the therapeutic use of ADSCs may also become
a reality for this continent.
Conclusion
Our view of adipose tissue has changed over time. Additional
information has led us to confirm that fat is not only a store of
energy, but when in excess, it is the instigator of obesity-related
co-morbidities. The characterisation of adipokines has led to the
realisation that adipose tissue is a true endocrine organ, and the
isolation and use of ADSCs has led to hope for future therapeu-
tic treatments of degenerative diseases of fat, bone, muscle and
cartilage. Once fat was just fat, but it is now much more than
that.
References
1.
Mathers CD, Boerma T, Ma FD. Global and regional causes of death.
Br Med Bull
2009;
92
: 7–32.
2.
Tipton CM. Historical perspective: the antiquity of exercise, exercise
physiology and the exercise prescription for health.
Wld Rev Nutr Diet
2008;
98
: 198–245.
3.
Cheng TO. Hippocrates and cardiology.
Am Heart J
2001;
141
:
173–183.
4.
Woodhouse R. Obesity in art: a brief overview.
Front Horm Res
2008;
36
: 271–286.
5.
Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and
obesity in the United States: prevalence and trends, 1960–1994.
Int J
Obes Relat Metab Disord
1998;
22
: 39–47.
6.
Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal
KM. Prevalence of overweight and obesity in the United States, 1999–
2004.
J Am Med Assoc
2006;
295
: 1549–1555.
7.
Abubakari AR, Lauder W, Agyemang C, Jones M, Kirk A, Bhopal RS.
Prevalence and time trends in obesity among adult West African popu-
lations: a meta-analysis
. Obes Rev
2008;
9
: 297–311.
8.
Wang Y, Mi J, Shan XY, Wang QJ, Ge KY. Is China facing an obesity
epidemic and the consequences? The trends in obesity and chronic
disease in China.
Int J Obes
(Lond)
2007;
31
: 177–188.
9.
Holdsworth M, Gartner A, Landais E, Maire B, Delpeuch F. Perceptions
of healthy and desirable body size in urban Senegalese women.
Int J
Obes Relat Metab Disord
2004;
28
: 1561–1568.
10. Kissebah AH, Krakower GR. Regional adiposity and morbidity
. Physiol
Rev
1994;
74
: 761–811.
11. Hamdy O, Porramatikul S, Al Ozairi E. Metabolic obesity: the paradox
between visceral and subcutaneous fat.
Curr Diabetes Rev
2006;
2
:
367–373.
12. Frayn KN. Visceral fat and insulin resistance – causative or correlative?
Br J Nutr
2000;
83
(Suppl 1): S71–S77.
13. Sniderman AD, Bhopal R, Prabhakaran D, Sarrafzadegan N, Tchernof
A. Why might South Asians be so susceptible to central obesity and its
atherogenic consequences? The adipose tissue overflow hypothesis.
Int
J Epidemiol
2007;
36
(1): 220–225.
14. Sjostrom L, William-Olsson T. Prospective studies on adipose tissue
development in man.
Int J Obes
1981;
5
: 597–604.
15. Couillard C, Mauriege P, Imbeault P, Prud’homme D, Nadeau A,
Tremblay A,
et al
. Hyperleptinemia is more closely associated with
adipose cell hypertrophy than with adipose tissue hyperplasia.
Int J
Obes Relat Metab Disord
2000;
24
: 782–788.
16. Mendez-Sanchez N, Arrese M, Zamora-Valdes D, Uribe M. Current
concepts in the pathogenesis of nonalcoholic fatty liver disease
. Liver
Int
2007;
27
: 423–433.
17. Ravussin E, Smith SR. Increased fat intake, impaired fat oxidation,
and failure of fat cell proliferation result in ectopic fat storage, insulin
resistance, and type 2 diabetes mellitus.
Ann N Y Acad Sci
2002;
967
:
363–378.
18. Montani JP, Carroll JF, Dwyer TM, Antic V,Yang Z, Dulloo AG. Ectopic
fat storage in heart, blood vessels and kidneys in the pathogenesis of
cardiovascular diseases.
Int J Obes Relat Metab Disord
2004;
28
(Suppl
4): S58–S65.
19. Alessi MC, Poggi M, Juhan-Vague I. Plasminogen activator inhibi-
tor-1, adipose tissue and insulin resistance.
Curr Opin Lipidol
2007;
18
: 240–245.
20. Mertens I, Verrijken A, Michiels JJ, Van der PM, Ruige JB, Van Gaal
LF. Among inflammation and coagulation markers, PAI-1 is a true
component of the metabolic syndrome.
Int J Obes (Lond)
2006;
30
:
1308–1314.
21. Gottschling-Zeller H, Birgel M, Rohrig K, Hauner H. Effect of tumor
necrosis factor alpha and transforming growth factor beta 1 on plasmi-
nogen activator inhibitor-1 secretion from subcutaneous and omental
human fat cells in suspension culture
. Metabolism
2000;
49
: 666–671.
22. Juhan-Vague I, Vague P. Hypofibrinolysis and insulin-resistance.
Diabetes Metab
1991;
17
: 96–100.
23. Umemura S, Nyui N, Tamura K, Hibi K, Yamaguchi S, Nakamaru M,
et al
. Plasma angiotensinogen concentrations in obese patients.
Am J
Hypertens
1997;
10
: 629–633.
24. Van H, V, Ariapart P, Hoffstedt J, Lundkvist I, Bringman S, Arner P.
Increased adipose angiotensinogen gene expression in human obesity.
Obes Res
2000;
8
: 337–341.
25. Giacchetti G, Faloia E, Sardu C, Camilloni MA, Mariniello B, Gatti C,
et al.
Gene expression of angiotensinogen in adipose tissue of obese
patients.
Int J Obes Relat Metab Disord
2000;
24
(Suppl 2): S142–S143.
26. Massiera F, Bloch-Faure M, Ceiler D, Murakami K, Fukamizu A, Gasc
JM,
et al
. Adipose angiotensinogen is involved in adipose tissue growth
and blood pressure regulation.
Fed Am Soc Exp Biol J
2001;
15
(14):
2727–2729.
27. Martinovic I, Abegunewardene N, Seul M, Vosseler M, Horstick G,
Buerke M,
et al
. Elevated monocyte chemoattractant protein-1 serum
levels in patients at risk for coronary artery disease.
Circ J
2005;
69
:
1484–1489.
28. Verma S, Li SH, Wang CH, Fedak PW, Li RK, Weisel RD,
et al
. Resistin
promotes endothelial cell activation: further evidence of adipokine-
endothelial interaction.
Circulation
2003;
108
: 736–740.
29. Savage DB, Sewter CP, Klenk ES, Segal DG, Vidal-Puig A, Considine
RV,
et al
. Resistin / Fizz3 expression in relation to obesity and peroxi-
some proliferator-activated receptor-gamma action in humans.
Diabetes
1...,31,32,33,34,35,36,37,38,39,40 42,43,44,45,46,47,48,49,50,51,...60
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