advice · food · medical


I like to think that I’m a multi-faceted person so it would be intellectual suicide to constantly upload post after post about the same sorts of things. 

So for all the yo-yo dieters, med geeks (like me) or just those interested in finding out something new about how we perceive food, here’s a post for you, and hopefully you’ll enjoy it…

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 them 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 Gucci 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 unwittingly 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? And if so, how?

Ok. Let’s take a moment to digest the preceding sentences. Because I know right now you are wondering if you’ve read this correctly because the obvious answer is no, right? It is for this reason that I want to endeavour to redefine the social misconception of what is a healthy body and how it predisposes to ill health particularly type 2 diabetes mellitus.


The answer is yes. 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) 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. 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. This poorly understood obesity paradox involves dangerous distribution of adipose tissue-largely visceral fat.


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 takes place when there is an excess intake of food with high sugar and fat content with little or no exercise.

Visceral fat harbours an assortment of receptors for adipocytokines which contribute to the development of diabetes including: insulin, leptin, lactate and resistin.

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 or act as sensors in response to hypoglycaemia by reducing the production of insulin. 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 striated muscle which contributes to insulin resistance. Fatty acid mobilisation from adipose tissue, normally suppressed by insulin, itself becomes insulin resistant leading to an increase in lipolysis-essentially the cycle of doom! Furthermore insulin also stimulates glucose uptake and ketone metabolism within the muscles.

Leptin is created largely inside adipoctyes and secretory cells located in the stomach. It is produced relative to the amount of adipose tissue deposited so individuals with high levels of omental 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 transport of FFAs into the adipoctyes. 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 high lactate levels. If left untreated a potentially fatal condition termed lactic acidosis could develop.

Resistin is produced by adipoctyes 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.


I’m guessing you have heard a lot or at least some information in regards to diabetes however the issue still stands. 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 £1.3billion in 2002 alone. Despite this, in 2005 there was more than 200 million people with diabetes and the WHO predicts that this will increase to over 360milllion in 2030.

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 and the added factor of sedentary lifestyles lead to advance overstressing of beta cells (Type 2 Diabetes).  This endocrine disorder arises when the beta cells can no longer surmount insulin resistance so is unable to maintain glucose homeostasis.

An even more terrifying statistic is that if you are MONW and diagnosed with Type 2 Diabetes your mortality risk is double that of someone who is both diabetic and overweight.  Research on the subject of metabolic obesity and diabetes is at its premature stage but the presumption is that those who are overweight have an increased lean muscle mass that somehow protects them.

So there you go guys! It could not be anymore clearer. We are all in the same boat regardless of size or weight. As a student, with such a busy lifestyle, you really don’t have much time to take care of yourself. But one day we all just really have to decide to be more active and eat a balanced but exciting diet (myself included). The key is everything in moderation (I guess that’s the doctor in me coming to light lol)! 

And as a fellow food lover, I cannot say it’ll be easy but the question still remains…

Will you?


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