Linoleic Acid-Rich Oil Supplementation Increases Total and High-Molecular-Weight Adiponectin and Alters Plasma Oxylipins in Postmenopausal Women with Metabolic Syndrome.

BACKGROUND: The onset of menopause increases the risk of metabolic syndrome (MetS). Adiponectin is an adipokine associated with insulin sensitivity that is lower in people with MetS. Supplementing diets with linoleic acid (LA)-rich oil increased adiponectin concentrations and improved glucose control in women with type 2 diabetes. The effect of LA on adipokines, especially total and the bioactive form of adiponectin, high-molecular-weight (HMW) adiponectin, in women with MetS is unknown. OBJECTIVES: The aim of this study was to explore the effect of supplementation of the diet with an oil rich in LA on adipokines in women with MetS. The effect of the LA-rich oil (LA-oil) on oxylipins, key metabolites that may influence inflammation and metabolism, was also explored. METHODS: In this open-label single-arm pilot study, 18 postmenopausal nondiabetic women with MetS enrolled in a 2-phase study were instructed to consume LA-rich vegetable oil (10 mL/d) as part of their habitual diets. Women consumed an oleic acid-rich oil (OA-oil) for 4 wk followed by an LA-oil for 16 wk. Fasting concentrations of adipokines, fatty acids, oxylipins, and markers of glycemia and inflammation were measured. RESULTS: After 4 wk of OA-oil consumption, fasting glucose and total adiponectin concentrations decreased whereas fasting C-reactive protein increased. After 16 wk of LA-oil supplementation total and HMW adiponectin and plasma oxylipins increased. Markers of inflammation and glycemia were unchanged after LA-oil consumption. CONCLUSIONS: Supplementation with LA-oil increased total and HMW adiponectin concentrations and altered plasma oxylipin profiles. Larger studies are needed to elucidate the links between these changes and MetS.This trial was registered at clinicaltrials.gov as NCT02063165.

Blood level of adiponectin is positively associated with lean mass in women without type 2 diabetes.

OBJECTIVE: The objective of this study was to evaluate the relationship between blood levels of adiponectin and leptin with lean body and trunk adipose mass in women with and without type 2 diabetes mellitus (T2DM). METHODS: This cross-sectional study analyzed baseline data from five previous clinical studies involving postmenopausal women (n = 95). Body composition was assessed by dual-energy x-ray absorptiometry, and appendicular lean mass was calculated based on body mass index (ALMBMI). Adipokines and cytokines were measured by enzyme-linked immunosorbent assay. Linear mixed-effect models with a random study effect were used to investigate the relationship between predictors (eg, adiponectin, leptin), outcomes (eg, ALMBMI, trunk adipose mass), and co-variables (T2DM status, age, interleukin-6, and C-reactive protein). RESULTS: Postmenopausal women with T2DM had lower ALMBMI than those without T2DM. There was a positive association between blood adiponectin and ALMBMI in postmenopausal women without T2DM, but no association in those with T2DM. Blood leptin was negatively associated with ALMBMI for women regardless of T2DM diagnosis. Blood adiponectin was negatively associated, whereas blood leptin was positively associated with trunk adipose mass for the entire cohort. CONCLUSIONS: T2DM status moderated the relationship between blood adiponectin and ALMBMI, where blood adiponectin was positively associated with ALMBMI in postmenopausal women without T2DM, but not those with T2DM. Dysregulated metabolism in T2DM may contribute to lower muscle mass in women with T2DM, but future research is required to elucidate this mechanistic link. The negative association between blood leptin and ALMBMI was a novel finding. Future studies will need to more clearly define the relationship between these variables.

Incorporation of eicosapentaenioic and docosahexaenoic acids into breast adipose tissue of women at high risk of breast cancer: a randomized clinical trial of dietary fish and n-3 fatty acid capsules.

SCOPE: The fatty acid profile of dietary lipids is reflected in mammary adipose tissue and may influence mammary gland biology and cancer risk. To determine the effects of fish consumption on breast adipose tissue fatty acids, we conducted a study of fish versus n-3 PUFA supplements in women at increased risk of breast cancer. METHODS AND RESULTS: High risk women were randomized to comparable doses of marine n-3 PUFAs as canned salmon + albacore or capsules for 3 months. Pre- and posttreatment fatty acid profiles were obtained by GC. Dietary fish (n = 12) and n-3 PUFA capsules (n = 13) yielded increased eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in plasma (p < 0.0001), erythrocyte membranes (p < 0.0001), and breast fat (p < 0.01) at 3 months. Women taking capsules had higher plasma and erythrocyte membrane EPA changes (∼four versus twofold, p = 0.002), without significant differences in DHA. Increases in breast adipose EPA, DHA were similar for both groups. Higher BMI correlated with smaller changes in plasma, erythrocyte membrane EPA, and breast adipose EPA, DHA. Adherence was excellent at 93.9% overall and higher in the fish arm (p = 0.01). CONCLUSION: Fish provides an excellent source of n-3 PUFAs that increases breast adipose EPA, DHA similar to supplements and represents a well-tolerated intervention for future studies of the impact of n-3 PUFAs and dietary patterns on breast cancer.