Adiponectin and leptin may be early markers of microvascular complications in patients with Type 1 diabetes, Egyptian researchers believe.

Their conclusion is based on a clinical study involving 63 Type I diabetic patients receiving insulin therapy, who were aged 5??”17.5 years. Of these patients, 33 had microalbuminuria, which the researchers considered to indicate the presence of microvascular disease.

Interestingly, the study found that, compared with normoabluminuric patients, microalbuminuric patients had significantly higher adiponectin levels (20.7 vs 25.8 µg/ml) and significantly lower leptin levels (18.8 vs 10.4 ng/ml).

Adiponectin levels were also positively correlated with microalbuminuria concentrations, and in regression analysis, microalbuminuria was the only significant independent predictor of adiponectin levels.

By contrast, leptin was positively correlated with body mass index, blood pressure, and C-reactive protein levels and negatively correlated with blood glucose and glycated hemoglobin A_1c. None of these factors independently predicted leptin levels.

Moreover, the researchers found that the ratio of adiponectin to leptin was strongly correlated with levels of fasting plasma glucose, glycated hemoglobin A_1c, microalbuminuria, and serum creatine.

Writing in the journal Clinical Biochemistry, Shaymaa Yahya (National Research Centre, Cairo) and fellow researchers say that the unexpected positive correlation between adiponectin and microalbuminuria may be an adaptive mechanism that counteracts oxidative stress.

“It can be suggested from this study that adiponectin and leptin are more predictive for microvascular complications than low-grade inflammatory markers,” they write.

“Besides, we concluded that adiponectin/leptin ratio may be used as a better marker for microvascular complications than adiponectin or leptin alone, as adiponectin/leptin ratio was correlated positively with the microalbuminuria concentration and diabetic control indices.”

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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Average blood sugar level amounts are determined by a few factors. This article will list what those factors are and how to determine whether your body is operating with a normal blood glucose level and what you might expect for changes during the day.

Your blood glucose level usually starts out on the lower side in the morning and rises and falls during the day - primary due to your food intake. Food that is consumed that contains carbohydrates are converted to energy by the hormone insulin which is produced by the pancreas. As your body gets low on energy, blood sugar amounts in the bloodstream rise until insulin does its job. Once the the glucose is converted, blood glucose levels decrease to a more stable level. Within a few hours, however as the body needs more energy, the glucose levels are once again on the rise. Glucose levels stay at a higher level until once again another round of food and nutrients are consumed. Such is the cycle of someone with average blood sugar level amounts.

Problems occur, however when the body does not produce enough insulin to convert the glucose. As a result, the glucose stays in the bloodstream and can wreak havoc in the body if the condition of high glucose amounts persist. The average person who is not at risk for diabetes has a blood glucose level between 75 and 150 mg. This can also vary from person to person based on their weight and the amount of physical activity that he or she has in their life.

Treatment with growth hormone (GH) leads to moderate improvements in serum lipids in elderly men and women, but increases insulin resistance (IR), report researchers.

Administration of GH, sex-steroids, or a combination of the two to healthy, older men and women has been reported to have a beneficial influence on body composition and lipids, say Marc Blackman (Veterans Affairs Medical Center, Washington District of Columbia, USA) and colleagues.

However, they add: “Despite these favorable alterations in body composition and lipids, several studies have reported that GH administration elevates fasting glucose and insulin concentrations.“

For this study, Blackman and team recruited 57 women and 74 men, aged 72 years on average, who were all apparently healthy.

The women were given transdermal estradiol and oral medroxyprogresterone acetate (HRT) and the men intramuscular testosterone enanthate injections (testosterone) and/or GH for a period of 6 months.

As reported in the Journal of Endocrinology and Metabolism, the researchers found that GH, but not GH plus HRT, or HRT, increased IR in women. Similarly, GH and GH plus testosterone, but not testosterone, alone increased insulin resistance in men.

Treatment with GH significantly decreased low-density lipoprotein cholesterol levels in both men (by 0.3 mmol/l; 11.6 mg/dl) and women (by 0.5 mmol/l; 19.3 mg/dl). However, GH increased triglycerides by 0.3??”0.5 mmol/l (26.6??”44.3 mg/dl) in men and women, but this was only of marginal significance.

Of note, HRT decreased both total and LDL cholesterol levels, and testosterone decreased total, but not LDL cholesterol levels.

“Taken together our results indicate an increase in IR after GH administration similar to that observed in obese women and men treated with GH,” conclude Blackman et al.

“Whether longer-term GH administration would result in beneficial effects on glucose and insulin homeostasis in healthy older individuals, as reported in patients with adult GH deficiency, remains to be determined.”

They add: “Although our study period of 6 months was too short to infer the relevance of the observed changes in laboratory parameters to cardiovascular risk, much longer term GH therapy has not been shown to alter atherosclerotic changes in patients with adult GHD.”

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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