This informal CPD article The Fat That’s Hidden: Are You A “Skinny Latte”? Metabolic Obesity And Its Association With Insulin Resistance was provided by Dr Costanza McIntosh at Black Leaders, a Black Leadership Community for Professionals working in Healthcare.
Type 2 Diabetes is up to three times more likely to be diagnosed in black communities. It is evident that more research must be done to deduce the causes of this alarming statistic. Furthermore we must realise that how a person looks may not always be an accurate indicator of their health especially when we continue to apply ‘westernised’ health criteria and ideals based solely on Caucasian biology whilst ignoring other groups in society.
What is Metabolic Obesity?
Everyone knows that person. They’ll be sitting there, quite self-righteous clinging proudly to their skinny latte hoping that it makes up for the audacious array of junk they consumed over the weekend. Neither they nor you are a gym person and are most definitely not partial to the odd big Mac with large fries. But to society they’re ‘normal’-because they are a ‘nice’ size, ‘healthy’ weight and can quite easily slip into your skinny jeans, you know the ones gathering dust in the bottom of your closet. So you sit there pondering how on earth they keep so “trim”? But unknowingly you are both sadly mistaken because just like a skinny latte with its hidden sugar content, what seems healthy can be deceiving. Thus the following question has to be asked: can an individual be thin but overweight?
There are such instances where individuals can be a normal weight but metabolically obese (MONW). Approximately a fifth of the UK population have a healthy Body Mass Index (BMI) between 18.5 and 24.9kg/m 2 but have health issues which are typically associated with obesity, these include increased insulin resistance, and elevated insulin levels, and as a consequence increased predisposition to Type 2 Diabetes (Peters en KF et al, 2006). Traditionally physicians based the majority of their assessment of obese patients on BMI, however, this index accounts for excess body fat but does not account for distribution or for variations in ethnicity groups.
Visceral Fat-Nature’s Toxic “Waist” Dump
White adipose tissue is an endocrine organ that encompasses both subcutaneous fat and visceral fat. Subcutaneous adipose tissue resides underneath the skin but remains outside the abdominal cavity and is beneficial or virtually uninvolved in metabolism. Visceral adipose tissue on the other hand is metabolised by the liver and is mainly centralised around the abdomen chiefly around the vital organs. Central obesity can be a complication of excess visceral adiposity where the waist circumference in comparison to the hips is vastly increased. Accumulation can take place when there is an excessive intake of food with high sugar and fat content and precipitated further by living a predominately sedentary lifestyle.
Visceral fat harbours an assortment of receptors for adipocytokines which contribute to the development of Diabetes including insulin, leptin, lactate and resistin (Bays HE et al, 2008). Insulin is manufactured by secretory cells within the pancreas. These cells are called the Islets of Langerhans-more specifically beta cells that produce insulin in response to amplified levels of glucose in the peripheral blood.
This biological phenomenon is identified as secretion coupling. It inhibits the following processes within the hepatocytes: gluconeogenesis (where glucose is manufactured from sources apart from carbohydrates), ketogenesis (production of ketones) and glycogenolysis (where glucose is formulated from the breakdown of glycogen). It is also involved in the inhibition of lipolysis where lipids are converted to non-esterified fatty acids (NEFAs) within the adipocytes. NEFAs are the body’s primary source of energy fuel which leads to increased production of triglycerides within the liver. Insulin levels are affected in Type 2 Diabetes which increases lipolysis so NEFAs remain at dangerously high levels. These soaring levels of NEFAs prevent insulin-mediated glucose oxidation within the striated muscle which contributes to insulin resistance. Fatty acid mobilisation from adipose tissue, normally suppressed by insulin, becomes insulin resistant leading to an increase in lipolysis- essentially the cycle of doom!
Leptin is created largely inside adipocytes and secretory cells located in the stomach. It is produced relative to the amount of adipose tissue deposited so individuals with high levels of central fat produce more leptin than those with a reduced amount. This hormone regulates energy intake and energy expenditure so it allows the body to determine if it has reached satiety. In both normal obesity and central obesity leptin levels are elevated within the blood so the body gains resistance to its effects leading to what is known as leptin desensitisation i.e. two bacon butties rather than one. This makes it much harder to determine satiety which increases energy consumption despite reduced energy expenditure so more adipose tissue accumulates.
Both insulin and leptin regulate free fatty acids (FFAs) that enter and leave the adipose tissue so that only when insulin levels ascend there is the transport of FFAs into the adipocytes. This process is normally efficient but in the presence of metabolic disease or adipose- derived inflammation can be inadequately controlled.
Lactate is metabolised in a reaction catalysed by pyruvate dehydrogenase in the presence of oxygen. Diabetes inhibits this enzyme which accounts for higher lactate levels. If left untreated a potentially fatal condition termed lactic acidosis could develop.
Resistin is produced by adipocytes through gene activation. Some research has suggested a positive correlation between insulin resistance and serum resistin but its role in metabolism is yet to be identified. Factors such as the high metabolic activity involving these fat-derived hormones within visceral fat can promote pre-type 2 Diabetes.
What is Pre-Type 2 Diabetes and How Does it Predispose to Type 2 Diabetes?
Governments have invested millions possibly billions of pounds into promoting the prevention of Type 2 Diabetes since the advent of the obesity epidemic, with the total NHS cost of diabetes estimated in excess of 1.3 billion pounds in 2002 alone (Walness Report, 2002).
Despite this, in 2005 there were more than 200 million people with diabetes and the World Health Organisation also predicts that this will increase to over 360 million people in 2030 (WHO, 2006). An even more terrifying statistic is that if you are MONW and diagnosed with Type 2 Diabetes you are twice as likely to die from it in comparison to those who are both diabetic and overweight.
Pre-type 2 Diabetes arises when there is uncontrolled regulation of glucose within the blood due to partial dysfunction of beta cells. The continuation of a carbohydrate- dense diet as well as doing little exercise can lead to an overstressing of beta cells increasing the risk of poor glucose regulation.
I do hope that I have demonstrated that we are all in the same boat regardless of size or weight. My intention was to dispel the myth that what you don’t know can’t hurt you as there is no doubt that there is a strong relationship between the “hypertriglyceridaemic waist” phenotype and insulin resistance. Consequently, it is up to us to grasp that autonomy and decide to be more active and eat a balanced vibrant diet. Eating healthily doesn’t have to be what you’ve been led to believe. It is all about little changes which lead to lifelong habits and it doesn’t have to be bland either! You can still use flavour from beautiful herbs and spices in your cupboard, bake your food more often then you fry and if you can try to get yourself an air fryer. It’s also okay to treat yourself every so often and find a form of exercise that works for you even if it means putting on some of your favourite tunes to get you moving. It’s all about innovation, moderation and of course consistency.
Now is the time to make the change. Are you ready?
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