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Implications of obesity-associated diabetes
The consequences of obesity are serious. Obese individuals are predisposed to
a cluster of metabolic disturbances known as 'syndrome X' or the metabolic
syndrome, which comprises glucose intolerance (the inability to metabolize glucose
adequately), type 2 diabetes mellitus, hypertension, dyslipidaemia (high
triglyceride levels accompanied by a raised concentration of low-density lipoproteins
and diminished high-density lipoproteins), leading to an increased risk of
stroke and cardiovascular disease (Ramirez, 1997; Reaven 1988, 1995; Walker
2001). In addition, obesity is also a risk factor for some malignancies such
as endometrial cancer (Iemura et al., 2000). The more life-threatening, chronic
health problems have been categorized into four main areas by WHO. These
include: cardiovascular problems including hypertension, stroke and coronary
heart disease; conditions associated with insulin resistance, namely type 2 diabetes;
certain types of cancer; as well as gall bladder disease.
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Development of obesity-related type 2 diabetes
Weight increases, particularly in the adipose tissue depots when the amount of
energy (calories) consumed exceed energy used for exercise and metabolic processes.
This is known as 'positive energy balance' and the excess is stored as
white adipose tissue (Frayn et al., 1995; Gregoire et al., 1998). It terms of the
development of type 2 diabetes, this is largely observed as excessive consumption
of nutrients, which are high in caloric content. Both excess consumption of
macronutrients such as carbohydrates and lipids coupled with increasing adiposity
lead to the progression of type 2 diabetes mediated principally via their negative
influence on insulin action and intermediary metabolism (Hill and Peters, 1998;Kopelman and Hitman, 1998;Woods et al., 1998; Obici et al., 2002). |
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Fat distribution
Increasing evidence has accumulated to demonstrate that regional adiposity plays
a greater role in the development of diabetes, impaired glucose tolerance and
atherosclerosis than generalized obesity. This concept is not entirely new-Vague
first described it in 1956 (Vague, 1956).
Different patterns of obesity exist, central obesity in which there is an increase
in intra-abdominal fat, particularly abdominal subcutaneous and omental fat;
lower body obesity, which is characterized by fat stored predominantly in
subcutaneous regions of hips, thighs and lower trunk (Abate, 1996). It has been clearly shown that both an increase in fatness and
a preferential upper-body accumulation of fat is independently related to insulin
resistance (Clausen et al., 1996). Obese women with a greater proportion of
upper-body fat tended to be more insulin resistant, hyperinsulinaemic, glucoseintolerant
and dyslipidaemic than obese women with a greater proportion of
lower-body fat. |
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Ectopic fat storage: fat content in obesity
Positive energy balance produces an excess of triglyceride with storage in the
liver (Ryysy et al., 2000) and skeletal muscle (Goodpaster and Kelley, 1998;
Goodpaster et al., 1997, 2000; Shulman, 2000) which is subsequently followed
by insulin resistance, glucose, intolerance and diabetes. This similar effect is
also observed in patients with lipodystrophy characterized by a severe reduction
in adipose tissue with increased triglyceride storage in the liver and skeletal
muscle (Robbins et al., 1979, 1982) and subsequent type 2 diabetes disease.
These observations suggest that in either the obese or lipodystrophic state, adipose
tissue mass is unable to sequester dietary lipid away from the liver, skeletal
muscle or the pancreas. As a result, too much or too little adipose tissue mass
leads to ectopic fat storage and may further predispose individuals to insulin
resistance and finally type 2 diabetes. |
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Target setting
Goal-setting is a pre-requisite prior to the initialization of diet therapy. It is
essential to set a realistic target of weight loss in a fixed period of time, e.g.
5-10 per cent of body weight in 6 months. Patients should be advised that
achieving an 'ideal weight' for height, i.e. to give a BMI of <25 kg/m2 may not
be an achievable target, and that not achieving such an ideal weight should not be
seen as failure. |
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Obesity and the risk of type 2 diabetes
Several prospective studies have documented that obesity is probably the most
powerful predictor of the development type 2 diabetes (Knowler et al., 1981;
Colditz et al., 1990; Manson et al., 1992). However, not every obese subject
develops diabetes, i.e. obesity alone is not sufficient to cause type 2 diabetes;
there are other factors that considerably modify the effect of obesity on diabetes
risk. For instance, it is likely that genetic susceptibility to diabetes is a
necessary prerequisite for diabetes. This was demonstrated in the Pima Indians
in whom the incidence increases more steeply with body mass index (BMI) in
those whose parents have diabetes than in those who do not (Knowler et al.,
1981). Vice versa, in non-obese people the incidence of type 2 diabetes is
low in the middle-aged even in populations such as the Pima Indians where
the overall risk of the disease is very high. However, a large proportion of
the human populations possess genes that permit type 2 diabetes to develop,
well documented by a high prevalence of diabetes and impaired glucose regulation
among the elderly (DECODE Study Group, 2003; Qiao et al., 2003).
Age-specific incidence rates of diabetes were also shown to vary according to
BMI (kg/m2) in the Pima Indians (Knowler et al., 1981): in younger age groups
subjects with a high BMI have higher incidence rates than those with lower
BMI.
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Patterns of weight loss in diabetes
The obese diabetic patient provides a particular challenge in terms of achieving
sustainable weight loss. Thus, the presence of type 2 diabetes gives the patient
increased problems in achieving clinically significant weight loss. As an added confounder the natural history of weight alteration in the diabetic patient is for
this to slowly increase, the rate of increase being dependent on drug therapy used
(UK Prospective Diabetes Study Group, 1998), both insulin and sulphonylurea
increasing the rate of weight gain.
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Weight loss and maintenance,
On achieving sustainable weight loss and maintenance, it is important to
recognize the above and to relay this information to the patient to allow his/her
better understanding of energy metabolism. Clear and frank discussion with
patients in respect of difficulties in achieving and maintaining weight loss are
essential. The approach to the patient by the whole healthcare delivery team as
to the role of diet and lifestyle alteration needs to send the same message. It
is also important that non-verbal communication to patients from the diabetic
management team reinforces the verbal statements. Contradictory messages will
lead to patient confusion, lack of confidence, and ultimate failure in achieving
weight reduction and hence failure to achieve improved glycaemic control, blood
pressure and/or lipid parameters. |
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