Results from a small experimental study suggest that free fatty acids (FFAs) play a role in inducing insulin resistance and may be linked to atherogenic processes regulated by the expression of the cell surface scavenger receptor CD36.

“Abnormalities in lipid metabolism, as observed in obesity and Type 2 diabetes mellitus, result in chronic elevations of plasma FFA levels, which have been reported to contribute to the development of insulin resistance, inflammation, and endothelial dysfunction in diabetic and nondiabetic individuals,” say Sangeeta Kashyap and colleagues from the Cleveland Clinic Foundation in Ohio, USA.

Less is known about the in vivo mechanisms through which increased levels of FFAs promote endothelial dysfunction and atherogenesis, but the cell surface scavenger receptor CD36 is thought to facilitate transport of FFAs into cells.

Kashyap and team investigated the lipid-induced insulin resistance, endothelial dysfunction, and the capacity of monocytes to form foam cells through the action of scavenger receptor A (SRA) and CD36 in 10 healthy volunteers.

The participants underwent a 24-hour infusion of intralipid/heparin plus saline (0.5 ml/min) on two different occasions. This was followed by brachial artery reactivity testing and a euglycemic hyperinsulinemic (80 mU/kg/min) clamp to assess insulin sensitivity.

Blood was also taken 24 hours after the infusion to isolate and study monocytes and their surface expression and functionality (uptake of oxidized low-density lipoprotein [oxLDL]) of SRA and CD36.

Writing in the journal Obesity, the researchers report that the lipid infusion led to a two-fold increase in the level of serum FFAs and a reduction in glucose disposal from the whole body of around 20%. A slight impairment of endothelial-dependent vasodilation was also observed.

There was a mean 25% increase in the cell surface expression of CD36 on the extracted monocytes, but not in that of SRA. This increase in CD36 expression led to a 50% increase in uptake of oxLDL and was inversely correlated with glucose disposal, which is in agreement with previous study results reported by MedWire News.

“All these data taken together suggest that lipid-induced insulin resistance or lipotoxicity is associated with atherogenesis and inflammation associated with scavenger receptor CD36 expression,” conclude Kashyap et al.

They suggest: “Selective downregulation of mononuclear/macrophage CD36 expression and/or inhibition of CD36 function pharmacologically may be an effective therapeutic strategy to retard atherosclerosis accelerated by lipid-induced metabolic diseases.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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CD36 linked to insulin sensitivity and level of IL-6

The use of insulin as a treatment for diabetes may become more common as the American Diabetes Association’s new treatment algorithm places basal insulin as a possible second-line treatment strategy after lifestyle modification and onlinepharmacylist.net/110/1/Glucophage/”>Metformin. Beginning insulin as a form of treatment requires proper education regarding injection technique. However, even with proper education by a certified diabetes educator problems can still occur. Here are some of the most common problems I encounter at the diabetes care center where I serve as the diabetologist and medical director.

Painful injections:

• Review your technique with your nurse educator.
• Try injecting at a 45 angle; you may be hitting muscle.
• Be sure the alcohol has dried.
• Inject quickly.
• Check to be sure you have not bent the needle when removing the cap.
• Change to a smaller needle length and/or diameter (gauge).
• Be sure the insulin is not too cold.
• Try injecting in a different site.
• Do not use needles more than once.
• Try to relax the muscle below the injection site.
• Larger doses just hurt more-sorry.

Bubbles in your insulin syringe: They won’t harm you if they are injected into the subcutaneous space; however, they obviously take up space in the syringe and will cause an inaccurate dose. Here are suggestions for avoiding bubbles:

• Draw up your insulin slowly and steadily from the vial.
• Draw up two or three more units of insulin into the syringe than you need. If bubbles are present, flick the syringe with one of your fingers to make the bubbles rise to the top and once the bubbles are at the top or you can find no bubbles then push the extra units of insulin back into the vial.
• If bubble do appear you can inject all the insulin back into the vial and redraw the dose.

Bleeding at the site of injection:

• Do not rub the injection site.
• Apply light pressure with your finger to prevent bruising.
• If a bruise appears, then do not use that injection site again until the bruise resolves.
• Frequent bleeding may indicate poor technique or another medical problem; contact your healthcare provider and/or nurse educator.

Insulin is dripping from the pen needle after injection:

• Wait at least five seconds after you inject before removing the needle.
• For doses of 25 units or more, wait 10 seconds before needle removal.
• When using a needle with a larger bore than 29-gauge, i.e., 28 or lower, wait 10 seconds before removing the needle.
• Do not carry a pen with the needle attached. This causes air to enter the cartridge, thus slowing the time it will take to get the insulin dose.

Insulin is leaking from the injection site:

• Try using a longer needle.
• Try a different injection site.
• Be sure you release the pinch before you remove the needle from the skin.

The injection device is clogged:

• Small amounts of insulin may be caught in the needle from a previous use: Never re-use needles.
• There may be a clump in the insulin: If you use cloudy insulin, be sure to properly mix your insulin before drawing it up.
• Cloudy insulin can dry inside the needle or syringe if drawn up too far before the time of injection: Fill your syringe closer to the time of your injection.

If these solutions do not solve your problem you need to contact your diabetes educator or provider for further assistance.

Are you confused about diabetes and wondering how you ended up with it? And what are you supposed to do about it? There is so much different information given to you, your head is spinning. Firstly, let’s look at the main differences between type 1 and type 2 diabetes and the effect of type 2 on both the lean and obese person.

1. Type 1 Diabetes:

• is an auto-immune condition
• the beta cells of the pancreas are destroyed by the body’s own immune system
• very little or no insulin is available and daily insulin-injections are required for life
• onset is usually rapid

2. Type 2 Diabetes:

• it is understood to be brought on by lifestyle choices

in the lean person:

• the pancreas secretes less than normal amounts of insulin
• then fewer doors are opened for glucose to enter the muscle cells
• this results in blood sugar levels being higher than normal
• glycogen stores in the liver are mobilized then raising blood-sugars even further
• blood-sugars are elevated because the pancreas slowly and gradually stops producing insulin

in the obese or overweight person:

• even more than normal amounts of insulin could be secreted into the blood stream to compensate for increased resistance caused by extra fat around the waistline
• this causes the keyholes (insulin-receptors) to change their shape so that the keys (insulin-molecules) do not fit as well and fewer doors are then opened to allow blood glucose to pass through
• these high blood-sugars cause even more insulin to be secreted into the blood stream by the pancreas
• this build-up is known as insulin-resistance
• in time the pancreas becomes overworked and gradually becomes tired and fails to produce insulin
• glycogen stores in the liver may be mobilized to raise blood sugar levels even further
• blood-sugars are raised mostly because the pancreas tires and/or insulin-resistance

Signs and Symptoms:

• slow onset
• can vary from none to mild

Treatment:

• First stage: … diet and exercise; if obese weight loss
• Second stage: … diet and exercise plus insulin-stimulating medications. There is no real way of knowing when or if this stage will definitely occur
• Third stage: … diet and exercise plus tablets and/or insulin-injections

The biggest difference is in the treatment:

People in the type 1 category require insulin as their body is no longer producing it. Lean or obese people with type 2 diabetes need to find their particular food, exercise, or medication plan so that it translates into normal blood sugar levels in his or her body.