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Lactoferrin, Green tea, Milk thistle, Omega-7, and Testosterone

May 2016

By Life Extension


Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: a double-blinded, randomized, placebo controlled study.

tBACKGROUND: Purified palmitoleic acid (16-1; omega-7) has shown lipid-lowering and anti-inflammatory benefits in open label, epidemiologic, and animal studies. OBJECTIVE: Our objective was to perform the first randomized controlled trial of purified palmitoleic acid supplementation in humans. METHODS: Adults with dyslipidemia and evidence of mild systemic inflammation (high-sensitivity C-reactive protein [hs-CRP] between 2 and 5 mg/L) were randomly allocated to receive either 220.5 mg of cis-palmitoleic acid (n = 30) or an identical capsule with placebo (1000 mg of medium chain triglycerides, n = 30) once per day for 30 days. Participants were asked to maintain their current diet. Serum lipids and hs-CRP were drawn at baseline and study completion. RESULTS: At 30 days, there were significant mean (95% confidence interval [CI]) reductions in CRP (-1.9 [-2.3 to -1.4] mg/L), triglyceride (-30.2 [-40.2 to -25.3] mg/dL), and low-density lipoprotein (LDL) (-8.9 [-12.0 to -5.8] mg/dL), and a significant increase in high-density lipoprotein (HDL) (2.4 [1.5, 3.3] mg/dL) in the intervention group compared with control. These changes equated to 44%, 15%, and 8% reductions in CRP, triglyceride, and LDL respectively, and a 5% increase in HDL compared with control. CONCLUSIONS: Purified palmitoleic acid may be useful in the treatment of hypertriglyceridemia with the beneficial added effects of decreasing LDL and hs-CRP and raising HDL. Further study is needed to elucidate mechanisms and establish appropriate human doses.

J Clin Lipidol. 2014 Nov-Dec;8(6):612-7

Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes.

BACKGROUND: Studies have demonstrated the beneficial effect of palmitoleic acid (C16:1 n-7) on reducing muscle insulin resistance and preventing beta-cell apoptosis. However, the effect of palmitoleic acid on diabetes remains to be elucidated. The aim of this study was to examine the antidiabetic effect of palmitoleic acid in KK-Ay mice, a spontaneous model for studies of obese type 2 diabetes with low insulin sensitivity. METHODS: KK-Ay mice were orally administered vehicle, 300 mg/kg of palmitoleic acid, or 300 mg/kg of palmitic acid (C16:0) on a daily basis for 4 weeks. RESULTS: Palmitoleic acid reduced body weight increase, ameliorated the development of hyperglycemia and hypertriglyceridemia, and improved insulin sensitivity. In addition, hepatic characteristics were significantly affected, as weight of the liver and hepatic triglyceride levels were lower in the palmitoleic acid group when compared to the control (vehicle and palmitic acid groups). Oil red O staining clearly indicated reduced hepatic lipid accumulation in response to palmitoleic acid. Furthermore, palmitoleic acid down-regulated mRNA expressions of proinflammatory adipocytokine genes (TNFa and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver. CONCLUSIONS: These results suggest that palmitoleic acid improves hyperglycemia and hypertriglyceridemia by increasing insulin sensitivity, in part owing to suppressing proinflammatory gene expressions and improving hepatic lipid metabolism in diabetic mice.

Lipids Health Dis . 2011 Jul 21;10:120

Circulating palmitoleate strongly and independently predicts insulin sensitivity in humans.

OBJECTIVE: We investigated whether palmitoleate, which prevents insulin resistance in mice, predicts insulin sensitivity in humans. RESEARCH DESIGN AND METHODS: The fasting fatty acid pattern in the plasma free fatty acid (FFA) fraction was determined in 100 subjects at increased risk for type 2 diabetes. Insulin sensitivity was estimated during an oral glucose tolerance test (OGTT) at baseline and after 9 months of lifestyle intervention and measured during the euglycemic-hyperinsulinemic clamp (n = 79). RESULTS: Circulating palmitoleate (OGTT:F ratio = 8.2, P = 0.005; clamp:F ratio = 7.8, P = 0.007) but not total FFAs (OGTT:F ratio = 0.6, P = 0.42; clamp:F ratio = 0.7, P = 0.40) correlated positively with insulin sensitivity, independently of age, sex, and adiposity. High baseline palmitoleate predicted a larger increase in insulin sensitivity. For 1-SD increase in palmitoleate, the odds ratio for being in the highest versus the lowest tertile of adjusted change in insulin sensitivity was 2.35 (95% CI 1.16-5.35). CONCLUSIONS: Circulating palmitoleate strongly and independently predicts insulin sensitivity, suggesting that it plays an important role in the pathophysiology of insulin resistance in humans.

Diabetes Care. 2010 Feb;33(2):405-7.

Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPARa-dependent manner.

We investigated whether palmitoleic acid, a fatty acid that enhances whole body glucose disposal and suppresses hepatic steatosis, modulates triacylglycerol (TAG) metabolism in adipocytes. For this, both differentiated 3T3-L1 cells treated with either palmitoleic acid (16:1n7, 200 µM) or palmitic acid (16:0, 200 µM) for 24 h and primary adipocytes from wild-type or PPARa-deficient mice treated with 16:1n7 (300 mg·kg(-1)·day(-1)) or oleic acid (18:1n9, 300 mg·kg(-1)·day(-1)) by gavage for 10 days were evaluated for lipolysis, TAG, and glycerol 3-phosphate synthesis and gene and protein expression profile. Treatment of differentiated 3T3-L1 cells with 16:1n7, but not 16:0, increased basal and isoproterenol-stimulated lipolysis, mRNA levels of adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) and protein content of ATGL and pSer(660)-HSL. Such increase in lipolysis induced by 16:1n7, which can be prevented by pharmacological inhibition of PPARa, was associated with higher rates of PPARa binding to DNA. In contrast to lipolysis, both 16:1n7 and 16:0 increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose without affecting glyceroneogenesis and glycerokinase expression. Corroborating in vitro findings, treatment of wild-type but not PPARa-deficient mice with 16:1n7 increased primary adipocyte basal and stimulated lipolysis and ATGL and HSL mRNA levels. In contrast to lipolysis, however, 16:1n7 treatment increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose in both wild-type and PPARa-deficient mice. In conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPARa.

Am J Physiol Endocrinol Metab . 2013
Nov 1;305(9):E1093-102

Palmitoleic acid (n-7) increases white adipocytes GLUT4 content and glucose uptake in association with AMPK activation.

BACKGROUND: Palmitoleic acid was previously shown to improve glucose homeostasis by reducing hepatic glucose production and by enhancing insulin-stimulated glucose uptake in skeletal muscle. Herein we tested the hypothesis that palmitoleic acid positively modulates glucose uptake and metabolism in adipocytes. METHODS: For this, both differentiated 3 T3-L1 cells treated with either palmitoleic acid (16:1n7, 200 µM) or palmitic acid (16:0, 200 µM) for 24 h and primary adipocytes from mice treated with 16:1n7 (300 mg/kg/day) or oleic acid (18:1n9, 300 mg/kg/day) by gavage for 10 days were evaluated for glucose uptake, oxidation, conversion to lactate and incorporation into fatty acids and glycerol components of TAG along with the activity and expression of lipogenic enzymes. RESULTS: Treatment of adipocytes with palmitoleic, but not oleic (in vivo) or palmitic (in vitro) acids, increased basal and insulin-stimulated glucose uptake and GLUT4 mRNA levels and protein content. Along with uptake, palmitoleic acid enhanced glucose oxidation (aerobic glycolysis), conversion to lactate (anaerobic glycolysis) and incorporation into glycerol-TAG, but reduced de novo fatty acid synthesis from glucose and acetate and the activity of lipogenic enzymes glucose 6-phosphate dehydrogenase and ATP-citrate lyase. Importantly, palmitoleic acid induction of adipocyte glucose uptake and metabolism were associated with AMPK activation as evidenced by the increased protein content of phospho(p)Thr172AMPKa, but no changes in pSer473Akt and pThr308Akt. Importantly, such increase in GLUT4 content induced by 16:1n7, was prevented by pharmacological inhibition of AMPK with compound C. CONCLUSIONS: In conclusion, palmitoleic acid increases glucose uptake and the GLUT4 content in association with AMPK activation.

Lipids Health Dis. 2014 Dec 20;13:199