The association between obesity and type 2 diabetes has been thoroughly researched. The basis for this link is the ability of obesity to cause insulin resistance. Insulin resistance is the fundamental aspect of type 2 diabetes and is also linked to a wide array of other health complications such as hyperlipidemia, hypertension, and atherosclerosis (American Diabetes, 2016). Although a lot of the details by which obesity causes insulin resistance remains unknown, there are variables such as dietary fatty acids, intramyocellular lipids, and central adiposity that have been studied to determine the association.
Insulin is a hormone produced by the beta cells in the pancreas which acts as the primary regulator of fat, protein, and most notably carbohydrate metabolism (Sears & Perry, 2015). Insulin regulates carbohydrate metabolism by acting as a gateway to allow blood glucose to enter the cells throughout the body. If the cells develop the inability to respond to insulin and take up blood glucose, it is known as insulin resistance. Other roles that insulin has include stimulating lipogenesis, diminishing lipolysis, increasing amino acid transport into cells, and DNA synthesis (National Institute, 2014). Due to many roles insulin plays in the body, it is important for insulin to be work properly.
Inflammation is a series of molecular and cellular responses that are responsible for defending the body from infections and other insults (Lee & Lee, 2014). It was first suggested that inflammation may be a contributor to insulin resistance when it was observed that certain anti-inflammatory drugs were effective in reducing blood glucose levels in diabetics (Sears & Perry, 2015). Some of this inflammation may be induced by the intake of pro-inflammatory fatty acids such as omega-6 and saturated fatty acids (Sears & Perry, 2015).
It appears that insulin resistance starts in the hypothalamus by disrupting the balance of hunger and satiety signals, which can lead to the overconsumption of calories (Sears & Perry, 2015). Both saturated fat and excess calories can cause inflammation of the hypothalamus, leading to resistance of satiety signaling of insulin. In animal models high fat diets rich in saturated fatty acids appears to inflame the hypothalamus within 24 hours. On the other hand, omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) which have anti-inflammatory properties, appears to have the ability to function as necessary substrates and bind to specific proteins that can decrease insulin resistance in an organ (Sears & Perry, 2015). These finding seem to support the position statement of the American Diabetic Association (ADA) stating that the type of fatty acids consumed is more important than the amount (Evert et al., 2014).
Skeletal muscle contributes of about 75% of the body’s glucose uptake (Corcoran, Lamon-Fava, & Fielding, 2007). Insulin resistance has been linked to the accumulation of intramyocellular lipid droplets within the skeletal muscle (Corcoran, Lamon-Fava, & Fielding, 2007). It is thought that lipid droplets provide a steady supply of fatty acid substrates that directly interfere with insulin signaling discouraging intracellular use of blood glucose (Muoio, 2012). This assumption has not always been validated in studies. There has been opposing studies that have found improvements in skeletal insulin sensitivity with little to no changes in intramyocellular lipid concentrations and even increased insulin sensitivity with increased intramyocellular lipid concentrations. Endurance athletes also seem to have high levels of intramyocellular lipid concentrations without experiencing insulin resistance, which is known as the ‘”athlete’s paradox” (Corcoran, Lamon-Fava, & Fielding, 2007). This paradox implies that it’s not necessarily the size of the intramyocellular lipid pool, but rather the balance between oxidation, cellular uptake, and fatty acid availability. Endurance exercise also seems to produce anti-inflammatory effects, reduce lipid peroxidation of skeletal muscle, and reduced deleterious lipid metabolites (Corcoran, Lamon-Fava, & Fielding, 2007).
Adipose tissue dysfunction is another factor plays a role in obese individuals developing insulin resistance (Snel et al., 2012).The accumulation of adipose tissue around the midsection area or central adiposity is an important contributor to insulin resistance. This condition results from chronic physical inactivity and overconsumption of calories. Central adiposity occurs both as subcutaneous fat (under the skin) or visceral fat (around the organs). This has led to the debate of whether abdominal subcutaneous fat or visceral fat is more strongly associated with insulin resistance (Snel et al., 2011). In a cohort study, excessive visceral fat was more associated with insulin resistance compared to subcutaneous fat. One reason could be the peptide adiponectin, which is suppressed by excessive visceral fat. When released by adipose tissues, adiponectin increases insulin sensitivity, has beneficial effects on lipid metabolism and postprandial glucose levels, and acts as protective factor for cardiovascular disease (Balsan, Vieira, Oliveira, & Portal, 2015). So the key seems to be decreasing visceral fat and calorie restriction has been shown to accomplish that as well as decrease the amounts of intramyocellular lipids in skeletal muscle (Hardy, Czech, & Corvera, 2012).
Obesity is a serious worldwide problem and is one of the main contributors to insulin resistance. Variables such as fatty acid consumption, intramyocellular lipid concentration, and central adiposity are connected within the dynamic of obesity and insulin resistance. Even though the exact mechanisms of these variables are still being discovered, it seems that diet composition, physically activity, and calorie restriction play important roles.
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By: Germaine Guy, RD, LDN