2. What is Metabolic
Syndrome?
Metabolic syndrome is a cluster of conditions —
increased blood pressure, high blood sugar, excess
body fat around the waist, and abnormal cholesterol
or triglyceride levels — that occur together,
increasing risk of heart disease, stroke and diabetes.
4. Risk factors
The following factors increase metabolic syndrome:
Age. metabolic syndrome increases with age.
Race. In the United States, Mexican-Americans appear to be at the
greatest risk of developing metabolic syndrome.
Obesity. Carrying too much weight, especially in abdomen, increases
risk of metabolic syndrome.
Diabetes. more likely to have metabolic syndrome if women had
diabetes during pregnancy (gestational diabetes) or if have a family
history of type 2 diabetes.
Other diseases. risk of metabolic syndrome is higher if their is
cardiovascular disease, nonalcoholic fatty liver disease or polycystic
ovary syndrome.
5. The major features of metabolic syndrome
include
Central obesity
Hypertriglyceridemia
Low high density lipoprotein (HDL)
Hyperglycemia
hypertension
6. Complications
Having metabolic syndrome can increase your risk
of developing:
Diabetes. If you don't make lifestyle changes to
control your excess weight, which can lead to
insulin resistance, your glucose levels will continue
to increase. You then might develop diabetes.
Cardiovascular disease. High cholesterol and high
blood pressure can contribute to the buildup of
plaques in your arteries. These plaques can narrow
and harden your arteries, which can lead to a heart
attack or stroke.
7. Are Helminthes Infections Associated with
Metabolic Syndrome?
• Numerous studies have shown an inverse
association between helminth infections and
inflammatory diseases such as allergies,
autoimmunities, and inflammatory bowel
disease, but importantly there is emerging
evidence that helminths seem to also be
associated with a lower incidence of MetS
8. What Is the Possible Mechanism behind the Association
between Helminths and Metabolic Syndrome?
Helminths need nutrients from their host for their growth and reproduction, and
this might use the energy of their host and therefore forestall obesity and insulin
resistance. However, helminths can also lead to the expansion of alternatively
activated Th2 and Treg. Th2 cytokines result in increased eosinophilia (EO) and,
when in adipose tissue, can lead to the alternative activation of macrophages in
this metabolically active organ; the AAMs in turn release anti-inflammatory
cytokines such as IL-10. The signaling pathways are currently being dissected, but
so far there is evidence that this cascade of events involves the activation of PPAR,
STAT6, and/or Akt. Moreover, it has been noted that when the immune system is
exposed to chronic helminth infections, EO and MCs no longer behave as pro-
inflammatory immune cells, and IgE under these conditions appears to be of low
affinity showing poor functional activity in terms of inducing MC degranulation.
Thus, in the presence of helminth infections, the immune system is in an anti-
inflammatory mode that is considered to be disadvantageous to the development
of T2D and CVD
9. What Is the Possible Mechanism behind the Association
between Helminthes and Metabolic Syndrome?
10. protective association between previous helminth
infections and metabolic disease has identified
three :plausible mechanisms
• A nutrition-based hypothesis is that the helminth
causes depletion of human energy sources
resulting in weight loss, leading to improved
metabolic outcomes. Infection was associated
with a significantly lower BMI. obesity is
associated with increased production of
proinflammatory cytokines that contribute to
insulin resistance, whereas nematode infections
induce strong Th2 and T regulatory cell responses
that can downregulate Th1/Th17-dependent
immunity,
12. • Alterations to the gut microbiome
Helminths may improve insulin sensitivity in the host
through manipulation of the human gut microbiome.
Animal studies of autoimmune disease have shown a
correlation between disease activity, helminth infection
and parallels in the qualitative and quantitative diversity
of the gut microbiome. So far, these studies have focused
on idiopathic chronic diarrhoea, ulcerative colitis, and
coeliac disease . A number of observational studies and
one randomised controlled trial have shown that changes
to the gut microbiome can improve insulin resistance.
The relationship between helminths, the microbiome and
metabolic outcomes has yet to be studied.
13. • Immunomodulation
It is postulated that helminth infections may
exert an evolutionary advantage by maintaining
host immune tolerance through immune-
modulation pathways.
14.
15. the possible protective effect against MetS of living in areas where
helminths are highly endemic is based on the presence of strong
anti-inflammatory and modified responses
To test this hypothesis, sufficiently powered longitudinal studies are
needed in the form of a randomized, double-blind, anthelmintic-
placebo-controlled trial that can reveal whether deworming leads
to MetS. Another method would be to infect patients with MetS
with helminths to assess whether the treatment can improve MetS.
Only then will it be possible to bridge the gap between the findings
in animal models and the situation in humans. Next, it might be
interesting to test which helminths or which of their products can
be used to modify inflammatory responses as a treatment for T2D
or CVD, as is currently being done in the field of allergy,
autoimmunity, and inflammatory bowel diseases.
•
Editor's Notes
Peroxisome proliferator-activated receptors (PPARs) (mainly present in adipose tissue, colon and macrophages) PPAR activation through binding of the synthetic TZDs(Thiazolidinedione
The term usually refers to a family of drugs used in the treatment of diabetes mellitus type 2 that were introduced in the late 1990 TZDs(Thiazolidinedione
STATs (signal transducers and activators of transcription) are transcription factors that provide a direct link between the cytokine
receptors and cytokine induced gene transcription.
is a human gene
Akt, is a serine/threonine-specific protein kinase that plays a key role in multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription and cell migration