Contribution of visceral fat mass to the insulin resistance of aging

Cefalu, William T.; Wang, Zhong Q.; Werbel, Sandra S.; Bell-Farrow, Audrey D.; Crouse, John R.; Hinson, William H.; Terry, James G.; Anderson, Randy L.

doi:10.1016/0026-0495(95)90251-1

Cited by 203 publications

(115 citation statements)

References 24 publications

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“…Insulin resistance often is related to increases in visceral adiposity, which is commonly observed with aging. 28 In this study, however, waist circumference was not shown to be a correlate of weight gain or a significant predictor in the multivariate analysis. Adjusting for baseline waist circumference had no effect on the relationship between insulin resistance and weight gain.…”

Section: Discussioncontrasting

confidence: 70%

Insulin resistance and weight gain in postmenopausal women of diverse ethnic groups

et al. 2004

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and 9 Women's Health Initiative, Southeast Region, Winston-Salem, NC, USA OBJECTIVE: This study was conducted to examine the influence of insulin resistance on weight change in postmenopausal women of various ethnic groups. SUBJECTS: Data were obtained from 3389 women (60% White, 20% Black, 12% Hispanic, and 8% Asian/Pacific Islander), ages 50-79, enrolled in either the Women's Health Initiative Clinical trial or Observational Study, whose blood samples were selected randomly from the full cohort of 161 809 women for analyses. MEASUREMENTS: Glucose, insulin, and lipids were measured on fasting serum samples drawn at baseline and after 3 y of follow-up. Weight, height, waist circumference, and blood pressure were measured. Physical activity and energy intake were assessed via questionnaire. Insulin resistance was estimated using the HOMA (homeostasis model) calculation. RESULTS: Average age was 62 y, average BMI (body mass index) was 27.4 kg/m 2 , and average weight change was a gain of 0.4 kg in 3 y. In a multivariate analysis, insulin resistance and insulin concentrations were independent predictors of increases in weight in White women (P ¼ 0.002 and 0.004, respectively) and in the combined group (P ¼ 0.027 and 0.039). For the whole group, after adjustment for other covariates, those in the highest quartile of insulin resistance gained 0.4 kg in 3 y, whereas those in the lowest quartile lost 0.06 kg. Similar trends were found for insulin resistance and weight gain in Hispanic and Asian/Pacific Islander women, but they did not reach statistical significance. In Black women, no relation was seen between either insulin or insulin resistance and weight change. A significant interaction between obesity and insulin resistance was observed (P ¼ 0.002 for White women and 0.032 for the whole group), so that there is weight gain with increasing insulin resistance in the leaner women, but weight loss with increasing insulin resistance in the most obese. CONCLUSION: Insulin resistance appears to be a predictor of weight gain in postmenopausal women, except for the most obese women. The effect is more pronounced in women who have a lower BMI, and the effect was not seen in the Black women who as a group had a higher BMI.

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Section: Discussioncontrasting

confidence: 70%

Insulin resistance and weight gain in postmenopausal women of diverse ethnic groups

et al. 2004

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“…29,30 In adolescent girls, visceral fat was a signi®cant correlate of insulin-mediated glucose disposal in obese but not in lean subjects. 31 Secondly, this population was younger than that studied by Cefalu et al 13 They studied a population in whom half the women were aged 60 ± 80, a much higher proportion than in our study. They also reported that intra-abdominal fat mass increases with advancing age, a ®nding that is con®rmed by our data ( Figure 2).…”

Section: Discussioncontrasting

confidence: 54%

Body fat distribution and cardiovascular risk in normal weight women. Associations with insulin resistance, lipids and plasma leptin

Tai

Lau

et al. 2000

Int J Obes

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OBJECTIVE: To systematically examine the correlations between insulin resistance, plasma leptin concentration, obesity and the distribution of fat assessed by anthropometry and magnetic resonance imaging in Asian women. DESIGN: A cross sectional study of non-diabetic, normal weight women. SUBJECTS: Twenty-one healthy women aged 38.8 y (s.d. 11.7) and BMI 22.6 kgam 2 (s.d. 2.3). MEASUREMENTS: Intraperitoneal, retroperitoneal and subcutaneous abdominal fat volume was assessed by magnetic resonance imaging. Anthropometric data were collected. Total fat mass was assessed by bioelectric impedance analysis. Fasting serum lipids, insulin and plasma leptin were assayed. RESULTS: Generalized obesity correlated with subcutaneous abdominal fat mass (r 0.83, P`0.001), but not with intra-abdominal fat mass. Both intraperitoneal fat mass and retroperitoneal fat mass increased with age (r 0.58, P 0.005 and r 0.612, P 0.003, respectively). Abdominal subcutaneous fat mass was the most important determinant of insulin resistance and plasma leptin. Of the serum lipids, only fasting triglyceride correlated signi®cantly with the waist-to-hip ratio. CONCLUSIONS: It is possible that the large size of the subcutaneous depot compared to the intra-abdominal depot overwhelms any metabolic differences between adipose tissue from these two sites, resulting in the stronger correlation between insulin resistance and subcutaneous abdominal fat mass rather than intra-abdominal fat mass. On the other hand, the distribution of fat between subcutaneous fat depots may be important in the metabolic syndrome given the correlation of fasting triglyceride with waist to hip ratio but not with abdominal fat. However, the study population was small, younger and leaner compared to previous studies and we may not be able to generalize these results to all segments of the population. We con®rm that subcutaneous fat mass is the major determinant of plasma leptin.

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“…An absolute or relative increase of body adiposity, particularly central body adiposity, often associated with advancing age, appears to account in large part for the age-related increase in insulin resistance (32,33). Even among adults without diabetes, intraabdominal fat mass correlates with insulin resistance and age after controlling for obesity (34). However, insulin resistance is more closely associated with abdominal adiposity than with age (35,36).…”

Section: Effects Of Agingmentioning

confidence: 92%

The Pathophysiology of Hyperglycemia in Older Adults: Clinical Considerations

2017

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Nearly a quarter of older adults in the U.S. have type 2 diabetes, and this population is continuing to increase with the aging of the population. Older adults are at high risk for the development of type 2 diabetes due to the combined effects of genetic, lifestyle, and aging influences. The usual defects contributing to type 2 diabetes are further complicated by the natural physiological changes associated with aging as well as the comorbidities and functional impairments that are often present in older people. This paper reviews the pathophysiology of type 2 diabetes among older adults and the implications for hyperglycemia management in this population.Diabetes is one of the leading chronic medical conditions among older adults, with high risk for vascular comorbidities such as coronary artery disease, physical and cognitive function impairment, and mortality. Despite decades of effort to prevent diabetes, diabetes remains an epidemic condition with particularly high morbidity affecting older adults. In fact, nearly 11 million people in the U.S. aged 65 years or older (more than 26% of adults aged 65 years or older) meet current American Diabetes Association criteria for diabetes (diagnosed and undiagnosed), accounting for more than 37% of the adult population with diabetes (1). At the same time, adults 65 years or older are developing diabetes at a rate nearly three-times higher than younger adults: 11.5 per 1,000 people compared with 3.6 per 1,000 people among adults aged 20-44 years old (1). However, increasing research in diabetes and aging has improved our understanding of the pathophysiology of diabetes and its association with aging and led to the development of a number of antihyperglycemic medications. The mechanism of diabetes complications has been previously reviewed (2). The current paper reviews the pathophysiology of type 2 diabetes among older adults and the implications for hyperglycemia management in this population. PATHOPHYSIOLOGY OF TYPE 2 DIABETESType 2 diabetes is by far the most prevalent form of diabetes in older adults and is an age-related disorder. The criteria for diagnosing diabetes are the same for all age groups because the risks of diabetes-related complications are associated with hyperglycemia over time across all age groups (3). Older adults are at high risk for the development of type 2 diabetes due to the combined effects of genetic, lifestyle, and aging influences. These factors contribute to hyperglycemia through effects on both b-cell insulin secretory capacity and on tissue sensitivity to insulin. The occurrence of type 2 diabetes in an older person is complicated by the comorbidities and functional impairments associated with aging.Hyperglycemia develops in type 2 diabetes when there is an imbalance of glucose production (i.e., hepatic glucose production during fasting) and glucose intake (i.e.,

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Contribution of visceral fat mass to the insulin resistance of aging

Cited by 203 publications

References 24 publications

Insulin resistance and weight gain in postmenopausal women of diverse ethnic groups

Insulin resistance and weight gain in postmenopausal women of diverse ethnic groups

Body fat distribution and cardiovascular risk in normal weight women. Associations with insulin resistance, lipids and plasma leptin

The Pathophysiology of Hyperglycemia in Older Adults: Clinical Considerations

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