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The vitamin D receptor polymorphism in the translation initiation codon is a risk factor for insulin resistance in glucose tolerant Caucasians
Ken C Chiu, Lee-Ming Chuang, Carol Yoon
BMC Medical Genetics , 2001, DOI: 10.1186/1471-2350-2-2
Abstract: There were 18 FF, 21 Ff, and 10 ff subjects. Since only 10 ff subjects were identified, they were pooled with the Ff subjects during analyses. The FF and Ff/ff groups had similar glucose levels at each time point before and after a glucose challenge. The Ff/ff group had higher insulin levels than the FF group at fasting (P=0.006), 30 minutes (P=0.009), 60 minutes (P=0.049), and 90 minutes (P=0.042). Furthermore, the Ff/ff group also had a larger insulin area under the curve than the FF group (P=0.009). While no difference was noted in %B, the Ff/ff group had a lower %S than the FF group (0.53 vs. 0.78, P=0.006). A stepwise regression analysis confirmed that the Fok I polymorphism was an independent determinant for %S, accounting for 29.3% of variation in %S when combined with waist-hip ratio.We report that the Fok I polymorphism at the VDR gene locus is associated with insulin sensitivity, but has no influence on beta cell function in healthy Caucasians. Although this polymorphism has been shown to affect the activation of vitamin D-dependent transcription, the molecular basis of the association between this polymorphism and insulin resistance remains to be determined.Although conflicting findings about bone mineral density (BMD) in patients with type 2 diabetes have been reported, there are substantial data which support the notion that type 2 diabetes is associated with increased BMD [1,2,3]. The Rotterdam Study [2], which involved 5,931 subjects, including 243 men and 355 women with type 2 diabetes, provides the most convincing evidence. They found that diabetic men and women had increased BMD independent of age, obesity, the use of estrogen, thiazide, or loop diuretics, impairment in the ability of daily living, and smoking [2]. Furthermore, hyperinsulinemia has been reported to be associated with an increased BMD in diabetic [4] and non-diabetic subjects [5]. From the Rancho Bernardo Study [5], the level of fasting insulin was significantly and positively assoc
Lipid and Fatty Acid Compositions of Chilling Tolerant Sweet potato (Ipomoea batatas L.) Genotypes  [PDF]
Shahidul Islam,Ehiorobo Izekor,James O. Garner
American Journal of Plant Physiology , 2012,
Abstract: Chilling injury is when morphological and physiological damage is sustained by plant tissue that is exposed to freezing temperatures. An experiment was conducted using four chilling tolerant sweet potato genotypes such as 105MS1, 108MS2, 180MS3 and 183MS4, which were selected from seventy nine lines from three major variety crosses for tolerant to chilling injury. The effects of chilling exposure on fatty acids compositions and peroxidase enzyme activity were studied. Chilling exposure increased the Peroxidase Enzyme Activity (PEA). Genotypes differences were also found in PEA following chilling exposure. All four genotypes that were tested had a high level (over 50%) of unsaturated fatty acid on their glycolipids. There were no differences found for the fatty acid percentage composition of the total glycolipid and phospholipid fractions from the four chilling tolerant genotypes except for C18:0 of the glycolipid fraction. However, C18:0 was found in low percentage and was not considered a major fatty acid. Sixty percent of total fatty acid in glycolipid fraction was C18:2 and C18:3. It was concluded that if lipids fatty acid composition was indeed a factor in chilling tolerance, it did not vary among the chilling tolerant genotypes. The result suggests that the genotypes were considered chilling tolerant to chilling environment, but that differences existed in their mechanism for tolerance. Thus, by breeding and selecting for chilling tolerance, it could enhance chilling tolerance in sweet potatoes.
N-3 fatty acids in glucose metabolism and insulin sensitivity
Martín de Santa Olalla,L.; Sánchez Muniz,F. J.; Vaquero,M. P.;
Nutrición Hospitalaria , 2009,
Abstract: polyunsaturated fatty acids (pufa) of the n-3 series are essential for normal growth and development. the health effects of these fatty acids include reduction of cardiovascular risk due to antiarrhythmic, antiinflammatory, anti-thrombotic and lipid lowering actions. an increase in unsaturation of the muscle membrane fatty acids is associated with improved insulin sensitivity. higher proportion of n-3 fatty acids may have beneficial roles, such as antiobesity effects and protection against the metabolic syndrome and type 2 diabetes mellitus through a number of metabolic effects. however, controversy exists on the different effects of n-6 and n-3 polyunsaturated fatty acids as well as on the interacting effect of dietary saturated and monounsaturated fat. in addition, some adverse effects have been described concerning the use of fish oil supplements containing high doses of n-3 fatty acids. several studies show eskimos diabetes risk, while results of nutritional interventions on the influence of consuming diets rich in oily fish or other food rich in n-3 fatty acids is very limited. this article reviews the possible mechanisms through which n-3 pufa are involved in glucose level control and insulin sensitivity. intervention and epidemiological studies together with recent findings on the nutrigenomic field related with this subject are also briefly reviewed.
Acute and second-meal effects of almond form in impaired glucose tolerant adults: a randomized crossover trial
Alisa M Mori, Robert V Considine, Richard D Mattes
Nutrition & Metabolism , 2011, DOI: 10.1186/1743-7075-8-6
Abstract: Fourteen impaired glucose tolerant (IGT) adults participated in a randomized, 5-arm, crossover design study where whole almonds (WA), almond butter (AB), defatted almond flour (AF), almond oil (AO) or no almonds (vehicle - V) were incorporated into a 75 g available carbohydrate-matched breakfast meal. Postprandial concentrations of blood glucose, insulin, non-esterified free fatty acids (NEFA), glucagon-like peptide-1 (GLP-1) and appetitive sensations were assessed after treatment breakfasts and a standard lunch.WA significantly attenuated second-meal and daylong blood glucose incremental area under the curve (AUCI) and provided the greatest daylong feeling of fullness. AB and AO decreased blood glucose AUCI in the morning period and daylong blood glucose AUCI was attenuated with AO. WA and AO elicited a greater second-meal insulin response, particularly in the early postprandial phase, and concurrently suppressed the second-meal NEFA response. GLP-1 concentrations did not vary significantly between treatments.Inclusion of almonds in the breakfast meal decreased blood glucose concentrations and increased satiety both acutely and after a second-meal in adults with IGT. The lipid component of almonds is likely responsible for the immediate post-ingestive response, although it cannot explain the differential second-meal response to AB versus WA and AO.The 2025 worldwide projection of IGT is 418 million (8.1% of the adult population) [1]. Lifestyle modification, including nutrition is the cornerstone of its management. Macro- and micronutrients, fiber content, and other components of the diet modulate meal-induced insulin secretion through changes in gastrointestinal transit time and nutrient absorption rates. Additionally, the content of one meal has the potential to affect insulin sensitivity at a second meal by altering circulating NEFA concentrations and daylong insulin demands [2].Almonds are a low-glycemic index (GI) food, with high fiber, unsaturated fat and low
Associations of Fatty Acids in Cerebrospinal Fluid with Peripheral Glucose Concentrations and Energy Metabolism  [PDF]
Reiner Jumpertz, Ana Guijarro, Richard E. Pratley, Clinton C. Mason, Daniele Piomelli, Jonathan Krakoff
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041503
Abstract: Rodent experiments have emphasized a role of central fatty acid (FA) species, such as oleic acid, in regulating peripheral glucose and energy metabolism. Thus, we hypothesized that central FAs are related to peripheral glucose regulation and energy expenditure in humans. To test this we measured FA species profiles in cerebrospinal fluid (CSF) and plasma of 32 individuals who stayed in our clinical inpatient unit for 6 days. Body composition was measured by dual energy X-ray absorptiometry and glucose regulation by an oral glucose test (OGTT) followed by measurements of 24 hour (24EE) and sleep energy expenditure (SLEEP) as well as respiratory quotient (RQ) in a respiratory chamber. CSF was obtained via lumbar punctures; FA concentrations were measured by liquid chromatography/mass spectrometry. As expected, FA concentrations were higher in plasma compared to CSF. Individuals with high concentrations of CSF very-long-chain saturated FAs had lower rates of SLEEP. In the plasma moderate associations of these FAs with higher 24EE were observed. Moreover, CSF monounsaturated long-chain FA (palmitoleic and oleic acid) concentrations were associated with lower RQs and lower glucose area under the curve during the OGTT. Thus, FAs in the CSF strongly correlated with peripheral metabolic traits. These physiological parameters were most specific to long-chain monounsaturated (C16:1, C18:1) and very-long-chain saturated (C24:0, C26:0) FAs. Conclusions: Together with previous animal experiments these initial cross-sectional human data indicate that central FA species are linked to peripheral glucose and energy homeostasis.
Modulation of Fatty Acid Oxidation and Glucose Uptake by Oxytocin in Adipocytes  [PDF]
Han-Jen Lin, Yu-Shan Chen, Yu-Jen Chen, Yuan-Yu Lin, Harry J. Mersmann, Shih-Torng Ding
Journal of Biomedical Science and Engineering (JBiSE) , 2017, DOI: 10.4236/jbise.2017.102005
Abstract: Oxytocin (OT) is a hypothalamic neuropeptide synthesized and secreted by OT neurons. In addition to its conventional role in reproductive physiology, central OT also regulates various social behaviors, such as care, trust, and emotions. Central and subcutaneous OT infusions stimulate lipid metabolism in mice and rats when fed standard or high fat diets. Mice lacking the OT receptor (OTR) or OT peptide develop late-onset obesity with greater fat pad weights, larger adipocyte size and elevated plasma levels of leptin. To study the effects of OT on lipid metabolism, we examined the effects of serial OT doses (0, 10, 30, 100, 150, 300 nM) on 3T3L1 adipocytes, together with long (144 hours, 6 days) and short (24 hours, 1 day) term treatments. The short-term treatment with 150 nM OT increased triacylglycerol (TAG) accumulation and decreased mRNA expressions of carnitine palmitoyltransferase 1α (CPT-1α) and fatty acid binding protein 4 (FABP4). After long-term incubation with 150 nM OT, only the CPT-1α mRNA was decreased. In differentiated adipocytes derived from pig adipose tissue stem cells, only hormone sensitive lipase mRNA was decreased after short- or long-term treatment with OT. To obtain further insight into the underlying mechanism of OT induction, we tested the involvement of the AKT/PKB pathway; however, AKT phosphorylation was decreased after treatment with 150 nM OT, suggesting that OT effects may be independent from the AKT/PKB pathway. Taken together, OT effects on adipocyte glucose and lipid metabolism are probably through mechanisms other than the AKT/PKB pathway.
Inhibitors of Fatty Acid Synthesis Induce PPARα-Regulated Fatty Acid β-Oxidative Genes: Synergistic Roles of L-FABP and Glucose  [PDF]
Huan Huang,Avery L. McIntosh,Gregory G. Martin,Anca D. Petrescu,Kerstin K. Landrock,Danilo Landrock,Ann B. Kier,Friedhelm Schroeder
PPAR Research , 2013, DOI: 10.1155/2013/865604
Abstract: While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone. Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor-α (PPARα) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity. Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure. High (20?mM) but not physiological (6?mM) glucose conferred on both TOFA and C75 the ability to induce PPARα transcription of the fatty acid β-oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice. However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose. These effects were not associated with an increased cellular level of unesterified fatty acids but rather by increased intracellular glucose. These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPARα in the context of high glucose at levels similar to those in uncontrolled diabetes. 1. Introduction Obesity and overweight are worldwide health problems, affecting >50% of the US population and exceeding tobacco as the major cause of preventable mortality in the USA [1–3]. Obesity is associated with the development of type 2 diabetes (NIDDM), cardiovascular disease, nonalcoholic fatty liver disease (NAFLD), and increased mortality [2, 4–7]. Consequently, increasing effort in therapeutics has focused on the development of drugs such as TOFA, C75, and cerulenin that target the fatty acid metabolic pathway to inhibit synthesis. C75 is a competitive irreversible, slow-binding inhibitor of fatty acid synthase (FASN), cerulenin is suicide inhibitor of FASN, and TOFA is an allosteric inhibitor of acetyl CoA carboxylase (ACC) [8–11]. While these agents lower whole body and adipose tissue weight, their mechanism(s) of action is not simply accounted for by inhibition of the FASN and ACC enzymes alone. Increased malonyl-CoA, for example, inhibits carnitine palmitoyl transferase 1A (CPT1A, the rate limiting enzyme in mitochondrial fatty acid β-oxidation) [8, 11]. Since the ACC inhibitor TOFA decreases malonyl CoA while the two FASN inhibitors (C75, cerulenin) increase malonyl-CoA, it was anticipated that TOFA would
Glucose-6-phosphate dehydrogenase regulation in the hepatopancreas of the anoxia-tolerant marine mollusc, Littorina littorea  [PDF]
Judeh L. Lama,Ryan A.V. Bell,Kenneth B. Storey
PeerJ , 2013, DOI: 10.7717/peerj.21
Abstract: Glucose-6-phosphate dehydrogenase (G6PDH) gates flux through the pentose phosphate pathway and is key to cellular antioxidant defense due to its role in producing NADPH. Good antioxidant defenses are crucial for anoxia-tolerant organisms that experience wide variations in oxygen availability. The marine mollusc, Littorina littorea, is an intertidal snail that experiences daily bouts of anoxia/hypoxia with the tide cycle and shows multiple metabolic and enzymatic adaptations that support anaerobiosis. This study investigated the kinetic, physical and regulatory properties of G6PDH from hepatopancreas of L. littorea to determine if the enzyme is differentially regulated in response to anoxia, thereby providing altered pentose phosphate pathway functionality under oxygen stress conditions. Several kinetic properties of G6PDH differed significantly between aerobic and 24 h anoxic conditions; compared with the aerobic state, anoxic G6PDH (assayed at pH 8) showed a 38% decrease in Km G6P and enhanced inhibition by urea, whereas in pH 6 assays Km NADP and maximal activity changed significantly between the two states. The mechanism underlying anoxia-responsive changes in enzyme properties proved to be a change in the phosphorylation state of G6PDH. This was documented with immunoblotting using an anti-phosphoserine antibody, in vitro incubations that stimulated endogenous protein kinases versus protein phosphatases and significantly changed Km G6P, and phosphorylation of the enzyme with 32P-ATP. All these data indicated that the aerobic and anoxic forms of G6PDH were the high and low phosphate forms, respectively, and that phosphorylation state was modulated in response to selected endogenous protein kinases (PKA or PKG) and protein phosphatases (PP1 or PP2C). Anoxia-induced changes in the phosphorylation state of G6PDH may facilitate sustained or increased production of NADPH to enhance antioxidant defense during long term anaerobiosis and/or during the transition back to aerobic conditions when the reintroduction of oxygen causes a rapid increase in oxidative stress.
High Physiological Omega-3 Fatty Acid Supplementation Affects Muscle Fatty Acid Composition and Glucose and Insulin Homeostasis in Obese Adolescents
Frida Dangardt,Yun Chen,Eva Gronowitz,Jovanna Dahlgren,Peter Friberg,Birgitta Strandvik
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/395757
Abstract: Obese adolescents have high concentrations of saturated fatty acids and low omega-3 long-chain polyunsaturated fatty acids (LCUFAs) in plasma phospholipids. We aimed to investigate effects of omega-3 LCPUFA supplementation to obese adolescents on skeletal muscle lipids and glucose and insulin homeostasis. Twenty-five obese adolescents (14–17 years old, 14 females) completed a randomized double-blind crossover study supplying capsules containing either 1.2 g omega-3 LCPUFAs or placebo, for 3 months each with a six-week washout period. Fasting blood glucose, insulin, leptin, adiponectin, and lipids were measured. Intravenous glucose tolerance test (IVGTT) and euglycemic-hyperinsulinemic clamp were performed, and skeletal muscle biopsies were obtained at the end of each period. The concentrations of EPA, DHA, and total omega-3 PUFA in muscle phospholipids increased in both sexes. In the females, omega-3 LCPUFA supplementation improved glucose tolerance by 39% (=0.04) and restored insulin concentration by 34% (=0.02) during IVGTT. Insulin sensitivity improved 17% (=0.07). In males, none of these parameters was influenced by omega-3 supplementation. Thus, three months of supplementation of omega-3 LCPUFA improved glucose and insulin homeostasis in obese girls without influencing body weight.
Triacylglycerol Fatty Acid Composition in Diet-Induced Weight Loss in Subjects with Abnormal Glucose Metabolism – the GENOBIN Study  [PDF]
Ursula Schwab, Tuulikki Sepp?nen-Laakso, Laxman Yetukuri, Jyrki ?gren, Marjukka Kolehmainen, David E. Laaksonen, Anna-Liisa Ruskeep??, Helena Gylling, Matti Uusitupa, Matej Ore?i?, for the GENOBIN Study Group
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002630
Abstract: Background The effect of weight loss on different plasma lipid subclasses at the molecular level is unknown. The aim of this study was to examine whether a diet-induced weight reduction result in changes in the extended plasma lipid profiles (lipidome) in subjects with features of metabolic syndrome in a 33-week intervention. Methodology/Principal Findings Plasma samples of 9 subjects in the weight reduction group and 10 subjects in the control group were analyzed using mass spectrometry based lipidomic and fatty acid analyses. Body weight decreased in the weight reduction group by 7.8±2.9% (p<0.01). Most of the serum triacylglycerols and phosphatidylcholines were reduced. The decrease in triacylglycerols affected predominantly the saturated short chain fatty acids. This decrease of saturated short chain fatty acid containing triacylglycerols correlated with the increase of insulin sensitivity. However, levels of several longer chain fatty acids, including arachidonic and docosahexanoic acid, were not affected by weight loss. Levels of other lipids known to be associated with obesity such as sphingolipids and lysophosphatidylcholines were not altered by weight reduction. Conclusions/Significance Diet-induced weight loss caused significant changes in global lipid profiles in subjects with abnormal glucose metabolism. The observed changes may affect insulin sensitivity and glucose metabolism in these subjects. Trial Registration ClinicalTrials.gov NCT00621205
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