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Abstract

Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes. In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells - the cells that release insulin - failure to control blood glucose levels results. Abnormalities in beta-cell function are therefore critical in defining the risk and development of type 2 diabetes. This knowledge is fostering exploration of the molecular and genetic basis of the disease and new approaches to its treatment and prevention.

OBJECTIVE:

to investigate whether increased insulin resistance is associated with a reduced risk of weight gain among Hispanic and non-Hispanic white persons in Colorado.
DESIGN:

measurements were taken at baseline and after an average of 4.3 years.
SUBJECTS:

789 normal glucose tolerant subjects 20 to 74 years of age were studied.
MEASUREMENTS:

fasting insulin levels were used as an indirect marker of insulin resistance.
RESULTS:

the average baseline body mass index (BMI) was 26.1 (+/- 3.6 s.d.) in men and 25.2 (+/- 4.4 s.d.) in women. The average weight change at follow-up was 0.8 kg (+/- 4.3 s.d.) in men and 1.3 kg (+/- 5.0) in women. A doubling in initial fasting insulin was associated with a reduced risk of gaining 5 kg (n = 134) and 10 kg (n = 24) of weight in logistic regression models (OR5kg = 0.76, 95% CI: 0.59, 0.99 and OR10kg = 0.61, 95% CI: 0.36, 1.02). Similarly, a doubling of initial fasting insulin was associated (P = 0.006) on average with a 6.3 kg less weight gain in linear regression models, independently of initial body weight, age, sex, ethnicity and BMI. The relation was consistently observed in men and women and in both ethnic groups.
CONCLUSION:

higher initial fasting insulin decreases the risk of subsequent weight gain in both Hispanic and non-Hispanic white normal glucose tolerant individuals similar to Pima Indians. This appears to be a common biologic characteristic in moderate to low as well as high risk populations for NIDDM.

In the last few years, there has been increasing interest in the physiological role of acylation-stimulating protein (ASP). Recent studies in rats and mice, in particular in C3 (−/−) mice that are ASP deficient, have advanced our understanding of the role of ASP. Of note, the background strain of the mice influences the phenotype of delayed postprandial triglyceride clearance in ASP-deficient mice. Administration of ASP in all types of lean and obese mice studied to date, however, enhances postprandial triglyceride clearance. On the other hand, regardless of the background strain, ASP-deficient mice demonstrate reduced body weight, reduced leptin and reduced adipose tissue mass, suggesting that ASP deficiency results in protection against development of obesity.

In humans, a number of studies have examined the relationship between ASP, obesity, diabetes and dyslipidemia as well as the influence of diet, exercise and pharmacological therapy. While many of these studies have small subject numbers, interesting observations may help us to better understand the parameters that may influence ASP production and ASP action.

The aim of the present review is to provide a comprehensive overview of the recent literature on ASP, with particular emphasis on those studies carried out in rodents and humans.