Cut the Waist

Cut the Waist

Illustrative photo for 'Cut the Waist'
The philosophy of Cut the Waist is to prevent obesity related ill health through education resources

Partitioning of body fat

Storage of fat in different compartments

The World Health Organisation defines obesity as "abnormal or excessive fat accumulation that presents risk to health".

It is increasingly recognised that the risk which excess body fat poses to health is dependent upon where that excess body fat, or adipose tissue, is stored. It is important to understand how the storage of body fat in various compartments can have an impact on health.

Body fat may be stored in the following compartments:

Individuals who have a tendency to accumulate of fat in the visceral compartment and in non-adipose tissue compartments such as the liver and heart may be regarded as having poor "fat health" which can result in adverse health consequences. We shall consider storage of body fat in each of the compartments in turn:

Subcutaneous adipose tissue

We have evolved to store body fat as fuel; an energy store, accumulated in times of plenty, in order meet our demands in times of need. Women have evolved a capacity to store excess body fat to cover the demands of both the mother and the nursing child for several years. The need to evolve a relatively long term body fat depot has meant that women in general have a greater capacity than men to expand the subcutaneous adipose tissue compartment.

Evolution therefore appears to have left its trace on our body fat distribution. Women tend to accumulate lower body fat, reflecting subcutaneous fat in the gluteo-femoral distribution. This gives a typical "pear shaped" or "gynoid" body shape.

Subcutaneous fat storage, particularly in the lower-body, "gynoid" distribution is generally considered to have a low association with the development of chronic disease such as type 2 diabetes and cardiovascular disease.

Obese yet metabolically normal individuals

Approximately 20% of people who meet the BMI criteria for obesity are insulin-sensitive and metabolically normal, despite having large amounts of body fat. These individuals are regarded as metabolically healthy but obese subjects (MHO) and are characterised by predominant subcutaneous adipose tissue accumulation.

The ability to expand the subcutaneous compartment in situations of positive energy balance may have a protective effect in preventing storage of fat in the visceral compartment and in non-adipose tissue such as liver and muscle. In this way, the subcutaneous adipose tissue acts in a somewhat protective manner - a "metabolic sink".

Weight gain is usually associated with the accumulation of excess body fat. A BMI within the overweight or obese range therefore most commonly indicates an excess of body fat.

Illustration of subcutaneous fat compartment

However BMI is a rather blunt tool for individual patient assessment as it gives no information regarding where the excess body fat is partitioned.

Other measurements are therefore necessary to assess the nature of body fat partitioning. This is particularly important in the assessment of individuals whom we suspect may be at risk of health consequences due to excess fat accumulation in high-risk depots such as the visceral compartment and in nonadipose tissue.

Visceral adipose tissue

Increased waist circumference measurement identifies individuals who have a tendency to store their body fat centrally.

Central adiposity is associated with the accumulation of visceral fat. Waist circumference measurement therefore provides a simple clinical tool to screen those who may have an expanded visceral fat compartment.

Illustration of the relationship between waist circumference and an expanded visceral fat compartment
BMJ 2001; 322: 716-720. Reproduced with permission from the BMJ Publishing Group.

Visceral fat represents a highly metabolically active adipose tissue compartment. Visceral fat undergoes an increased rate of lipolysis in relation to the more stable subcutaneous compartment.

The major secretory product of visceral fat is non esterified fatty acids (NEFA). An excess of NEFA promotes increased triglyceride synthesis by the liver. Raised fasting triglycerides particularly in association with raised waist circumference would therefore suggest visceral fat accumulation.

In addition to the supply of NEFA, visceral fat is also a source of many fat-derived hormones "adipocytokines" and inflammatory mediators which are associated with the development of insulin resistance, raised blood pressure and atherogenesis.

Illustration: Internal fat as a hormone factory

Illustration of visceral fat compartment

The "hypertriglyceridaemic waist" phenotype is a useful concept to characterise those who may be at risk of developing type 2 diabetes and cardiovascular disease as a result of a tendency to store excess body fat in the visceral compartment.

Expansion of the visceral fat compartment is associated with atherogenic dyslipidaemia.

Illustration of the 'hypertriglyceridaemic waist' phenotype

Viscerally obese yet normal weight individuals

18% population are metabolically obese but normal body weight i.e. may be normal weight or may be slightly overweight but exhibit a tendency to store body fat in high-risk sites.

These relatively normal weight individuals may be characterised by a reduced lean tissue (muscle) mass and raised waist circumference.

In such individuals BMI measurement can give false reassurance. More detailed assessment of these patients may uncover risk factors for heart disease and type 2 diabetes despite a relatively normal body weight.

Non-adipose tissue compartment (steatosis)

In obesity abnormal accumulation of body fat can occur in non-adipose tissue - organs such as liver, heart and skeletal muscle.

Non-alcoholic fatty liver disease (NAFLD)

The accumulation of fat in non-adipose tissue is called steatosis eg hepatic steatosis. Liver fat accumulation is also known as non-alcoholic fatty liver disease (NAFLD). NAFLD encompasses a spectrum of liver pathology associated with fat accumulation. In some cases these is evidence of an associated inflammatory response within the liver - non-alcoholic steatohepatitis (NASH).

Illustration of non-adipose tissue compartment

The most frequently encountered biomarker of fatty liver disease is an isolated raised ALT, particularly in association with a raised waist circumference. Although in NAFLD a raised ALT can occur in isolation, it is often encountered in the context of raised fasting triglyceride levels or possibly coexisting pre-diabetes or frank type 2 diabetes.

It is important to exclude other possible causes of abnormal liver function, particularly in cases where other biomarkers of liver disease are abnormal, prior to considering a diagnosis of NAFLD.

Cardiac steatosis

The development of sophisticated imaging techniques, such as magnetic resonance spectroscopy (MRS), has allowed both quantification of fat deposition within the heart muscle (myocardium) and correlation between heart function and extent of abnormal fat deposition.

Emerging evidence suggests that fat deposition in the form of excess triglyceride (TG) within heart muscle cells is associated with impaired cardiac function (diastolic dysfunction). Visceral fat accumulation is demonstrated to correlate with myocardial TG content, suggesting that measures of central adiposity such as waist circumference could serve as an indirect and inexpensive surrogate measure of myocardial TG content.

Due to the observed relationship between central adiposity and myocardial TG content, it could be postulated that lifestyle modification to reduce weight and waist circumference could result in reduction in myocardial TG content.

Skeletal muscle ectopic fat deposition

Skeletal muscle is designed to metabolise fatty acids as a predominant fuel supply, but has capacity to switch to metabolise glucose when this is available, for example after meals. Insulin produced in response to meal ingestion facilitates entry of glucose into skeletal muscle cells for utilisation and an energy source. This "dual fuel" system was first described by Sir Philip Randle and has been named the Randle Cycle.

An increase in fat deposition in skeletal muscle cells (intramyocellular lipid accumulation in the form of lipid metabolities diacylglycerol (DAG), Ceramide and fatty acyl CoA) interferes with insulin signalling and leads to insulin resistance.

As a result of excess lipid accumulation interfering with insulin function, skeletal muscle loses metabolic flexibility to metabolise glucose in those who are overweight or obese. Physical activity and weight loss are associated with improvements in muscle insulin sensitivity, demonstrating that it is possible to restore metabolic flexibility and improve glucose uptake and utilisation by muscle.

References

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Bays HE et al. Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity. Expert Rev. Cardiovasc. Ther. 2008; 6(3); 343-368

Lindsey JB Steatosis and myocardial dysfunction. Journal of the American College of Cardiology 2008; 53(22); 1800-1802

Kelley DE et al. Fuel selection in human skeletal muscle in insulin resistance. Diabetes 2000; 49: 677-683

Petersen KF et al. Etiology of insulin resistance. American Journal of Medicine 2006; 119(5A):10S-16S

Goodpaster BH et al. Enhanced fat oxidation through physical activity is associated with improvements in insulin sensitivity in obesity. Diabetes 2003; 52: 2191-2196