**9. Discussion**

Of the anthropometric measures Body mass index (BMI), waist circumference and waist-hip ratio, waist circumference were reported to be more closely related to abdominal obesity and T2DM. Majority of the studies supported the view that there is no optimal cut-off point that can be universally applied. It was suggested that country or region-specific cut off points may be used. [13-14]

Data available in the literature suggest that lower waist circumference and waist-hip ratio cut off point for Asians-85cm and 80 cm, W/H ratio 0.9 and 0.8 for men and women, respectively. [15-17] A study from Tunisia provided a cut‐off point for waist circumference (for obesity, diabetes,and CVD) of 85 cm for both men and women, based on sensitivity being equal to specificity.[18]. The values for BMI and WC for Arab Nations are reported to be similar to European population.[19]

Obesity is a major public health concern for Libya. It is reported that about 30% of Libyan adults are obese. About 64% of Libyan adults are either overweight or obese. In the present study BMI values for control subjects were 29.5, 34.5 for obese subjects and 36.50 for T2DM subjects. WC values for control was 104cm,114 cm for obese subjects and 120 for T2DM subjects. These values clearly indicate that majority of the population are either over-weight or obese. This is supported by data that obesity related diseases like type 2 diabetes (T2DM), hyperten‐ sion, poly cystic ovarian disease (PCOD) are on the rise in Libya. [7, 20-22]. There is a dire need for finding risk markers for obesity and obesity related disorders.

There is a shift in focus to find out whether ethnic diversity could be a factor in the distribution pattern of adiposity variation in different populations. Few studies have stated that adipocy‐ tokines particularly adiponectin values differ for different population indicating that adipo‐ nectin could be taken as a biomarker of ethnic heterogeneity. When compared to other population serum adiponectin values were comparatively lower for Libyan subjects. Serum leptin and resistin levels were higher for obese and T2DM subjects compared to control ones.Paradoxically the serum levels of adiponectin were higher for T2DM subjects contrary to reports that there is hypoadiponectinemia in T2DM. Hyperadiponectinemia reported quite contrary to the earlier observations is suggested to be due to the presence of severe insulin resistance possibly to genetically defective insulin receptors. [23]

This finding emphasizes that insulin receptor has a critical role regulating adiponectin synthesis as well as clearance. Patients who have anti-insulin receptor antibodies may be responsible for severe insulin resistance (Type B IR) who show a significant increase in serum adiponectin levels. Such a finding brings out considerable focus on the adiponectin –insulin sensitivity concept. Rather it opens up for more avenues of research to exactly elicit the adiponectin's role in insulin sensitivity and suggests that insulin effect on adiponectin metabolism is undermined.[23]

In the present study T2DM Libyan patients showed marked increase in serum adiponectin levels compared to the control subjects. These subjects had higher insulin levels and insulin resistance shown by HOMA index. The duration of diabetes in these patients is 10 years or more.The results are not shown here.

**9. Discussion**

\*France et al [12] \*\* present study

**Table 6.** Serum lipid profile in different ethnic groups

Total cholesterol (mg/dL)

110 Treatment of Type 2 Diabetes

HDL cholesterol (mg/dL)

be used. [13-14]

European population.[19]

Of the anthropometric measures Body mass index (BMI), waist circumference and waist-hip ratio, waist circumference were reported to be more closely related to abdominal obesity and T2DM. Majority of the studies supported the view that there is no optimal cut-off point that can be universally applied. It was suggested that country or region-specific cut off points may

Triglcyerides(mg/dL) 145.12±24.50 140.6±25.50 145.5±12.20 0.45

**\*Non-south Asians \*South Asians \*\*Libyan P value**

0.0028 <0.01

0.033 <0.05

207.60±30.45 199.88±28.45 \*128.45±18.40

47.55±6.50 41.45±8.50 \*37.5.±5.50

Data available in the literature suggest that lower waist circumference and waist-hip ratio cut off point for Asians-85cm and 80 cm, W/H ratio 0.9 and 0.8 for men and women, respectively. [15-17] A study from Tunisia provided a cut‐off point for waist circumference (for obesity, diabetes,and CVD) of 85 cm for both men and women, based on sensitivity being equal to specificity.[18]. The values for BMI and WC for Arab Nations are reported to be similar to

Obesity is a major public health concern for Libya. It is reported that about 30% of Libyan adults are obese. About 64% of Libyan adults are either overweight or obese. In the present study BMI values for control subjects were 29.5, 34.5 for obese subjects and 36.50 for T2DM subjects. WC values for control was 104cm,114 cm for obese subjects and 120 for T2DM subjects. These values clearly indicate that majority of the population are either over-weight or obese. This is supported by data that obesity related diseases like type 2 diabetes (T2DM), hyperten‐ sion, poly cystic ovarian disease (PCOD) are on the rise in Libya. [7, 20-22]. There is a dire need

There is a shift in focus to find out whether ethnic diversity could be a factor in the distribution pattern of adiposity variation in different populations. Few studies have stated that adipocy‐ tokines particularly adiponectin values differ for different population indicating that adipo‐ nectin could be taken as a biomarker of ethnic heterogeneity. When compared to other population serum adiponectin values were comparatively lower for Libyan subjects. Serum leptin and resistin levels were higher for obese and T2DM subjects compared to control ones.Paradoxically the serum levels of adiponectin were higher for T2DM subjects contrary to reports that there is hypoadiponectinemia in T2DM. Hyperadiponectinemia reported quite

for finding risk markers for obesity and obesity related disorders.

This finding appears unique to Libyan diabetic subjects. It is reported earlier that adiponectin levels in Libyan subjects are comparatively lower when compared to European or western population in general. Therefore serum adiponectin levels seem to be determined by ethnic heterogeneity reflected by the distribution of adipose tissue and its genetic regulation of adiponectin's synthesis, secretion and degradation. Possibly the reportedly higher BMI in the population with a higher basal insulin levels (accompanied by insulin resistance) might have an suppressive effect on adiponectin formation or clearance.

Insulin resistance(IR) is now generally accepted to be the primary metabolic defect of T2DM [24]. IR is defined as a state that requires more insulin to obtain the biological effects achieved by a lower amount of insulin in the normal state [25].

In contrast to other adipokines, circulating levels of adiponectin correlate inversely with body fat and IR in humans [26] and rodent models [25].). It circulates at high levels in human plasma accounting for approximately 0.01% (0.5-30 µg/mL) of all plasma protein in normal individuals [27], 1000-fold higher than other hormones such as leptin and insulin. Gender has an effect on concentrations of adiponectin, with females having higher levels than males [28]. It is also well known that adiponectin levels increase with age, however the cause for this increase is still unknown [29]

The molecule adiponectin is a 244-amino-acid long adipokine secreted from adipocytes. The gene product is a 30kD protein [30], however this is not found in circulation. Adiponectin automatically self-binds to form larger structures and there are different multimeric forms including low molecular weight (LMW) trimers, middle molecular weight (MMW) hexamers, high molecular weight (HMW) oligomeric structures and finally globular adiponectin (gC1q domain)[27]. It has been proposed that this globular fragment is generated by proteolytic cleavage of adiponectin multimers by leukocyte elastase secreted from activated monocytes and/or neutrophils [24]; however the pathophysiological importance of this cleavage remains to be determined. Structurally, the globular form of adiponectin lacks the collagenous domain necessary for multimerization. Adipocytes secrete both the low-molecular weight and highmolecular weight forms of adiponectin in vivo and in vitro. Thus, the low-molecular weight and high-molecular weight forms of adiponectin are the predominant forms in serum whilst smaller complexes such as the trimer are virtually undetectable. [31].
