scholarly journals Can dietary intervention produce long-term reductionin insulin resistance?

2000 ◽  
Vol 83 (S1) ◽  
pp. S169-S172 ◽  
Author(s):  
Jim I. Mann
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Dietary Fat ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Lifestyle Changes ◽  
Visceral Adiposity

Insulin sensitivity is potentially enhanced by a range of diet-related changes including reduction of visceral adiposity, a reduction in saturated fatty acids, and possibly a redistribution of the proportions of various unsaturated fatty acids. While there is evidence to suggest that lifestyle changes can reduce the risk of progression of impaired glucose tolerance to type 2 diabetes, there are no clinical trials which have conclusively demonstrated that any measure can reduce insulin resistance in the long term to an extent that can prevent the development of type 2 diabetes and other clinical complications. Evidence concerning the possibilities for reducing visceral adiposity and altering the nature of dietary fat are therefore considered. Attempts to achieve prolonged and substantial weight reduction in adults have not been encouraging, and it may be that preventing further weight gain is the most realistic target in this age group. In childhood the attempts have been more successful. The development of new approaches to achieving behavioural change and an environment which facilitates physical activity and appropriate food choices will be essential for more successful individual and population attempts to facilitate reduction in insulin resistance by weight loss. Changes in the nature of dietary fat appear to be more easily achieved. This is already a component of dietary advice aimed at cardiovascular risk reduction, and should be reinforced now with a view to also achieving a reduction in insulin resistance.

Disease Prevention through Lifestyle: A Case of the Copper to Zinc Ratio and Insulin Sensitivity

2021 ◽  
Vol 3 (2) ◽  
Author(s):  
Purnendu Nath ◽  
Sukhpreet Patel
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
High Ratio ◽  
Lifestyle Changes ◽  
Multiple Organs ◽  
High Copper

Both type 2 diabetes mellitus and a high ratio of copper to zinc are independently associated with comorbidities involving multiple organs. Separately, patients with poor insulin sensitivity are often reported as having high copper and low zinc. This article reports the case of a 46-year-old male patient interested in reversing his insulin resistance and high copper to zinc ratio, therefore reducing his long-term risk of Alzheimer’s disease. Over a period of 16 weeks, through lifestyle changes and controlling for copper in the patient’s food and water supply, the patient’s copper to zinc ratio improved from 1.91 to a healthy level of 0.55 and his HOMA-IR score improved from 2.0 to a nondiabetic level of 1.2.

scholarly journals The Ratio of Unsaturated to Saturated Fatty Acids is a Distinguishing Feature of NAFLD in Subjects With Metabolic Disease

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A421-A421
Author(s):  
John N Falcone ◽  
Maurice A Hurd ◽  
Sonal Kumar ◽  
Michele Yeung ◽  
Carolyn Newberry ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Liver Disease ◽  
Saturated Fatty Acids ◽  
The Other ◽  
Acid Index

Abstract Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease affecting at least a quarter of the world’s population. NAFLD is commonly associated with other metabolic conditions such as insulin resistance, type 2 diabetes, obesity, and dyslipidemia. Given the liver’s prominent role in regulating glucose and lipid homeostasis, we hypothesized that subjects with NAFLD have a distinct profile of blood analytes. This investigation examines the association between NAFLD and circulating markers of glucose and lipid metabolism in order to identify a NAFLD-specific metabolite panel that can be used as a predictive biomarker in future studies. We are performing a cross-sectional study in 500 subjects to identify genetic and hormonal factors that correlate with the presence of NAFLD. This abstract reports a preliminary analysis of the results from the first 45 subjects enrolled. Fasting blood samples were collected from 31 subjects with NAFLD and 14 subjects with other metabolic diseases (‘Other’) and without radiologic evidence of NAFLD. The following analytes were measured: serum alanine aminotransferase (ALT), total cholesterol, direct-LDL, HDL, triglycerides, ApoB, small dense LDL-C (sdLDL), VLDL, Lp(a), cholesterol absorption/production markers (beta-sitosterol, campesterol, lathosterol, and desmosterol), glucose, insulin, hemoglobin A1C, adiponectin, hs-CRP, and fatty acids (saturated and unsaturated). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated from glucose and insulin levels, and fatty acids were batched together by structural similarity and reported as indices. The groups were compared using multiple t-tests or the Kolmogorov-Smirnov test when data were non-parametric. The NAFLD group had a mean age 48.4 ± 12.9 yrs and BMI 32.9 ± 6.6 kg/m2. These participants were 61% female and 58% had dyslipidemia, 25% pre-diabetes, and 25% type 2 diabetes. The Other group had a mean age 49.9 ± 12.9 yrs and BMI 39.1 ± 15.6 kg/m2. They were 64% female and 57% had dyslipidemia, 14% pre-diabetes, and 21% type 2 diabetes. ALT was higher in the NAFLD group (55 ± 40 vs 27 ± 22 IU/L, P<0.001). Intriguingly, the saturated fatty acid index was elevated in the NAFLD group (32.5 ± 1.9 vs 30.1 ± 2.2 %, P<0.05), and the omega-6 fatty acid index was elevated in the Other group (42.9 ± 3.7 vs 38.5 ± 4.7 %, P<0.05). These changes led to an unsaturated/saturated fatty acid ratio that was significantly lower in the NAFLD group (2.0 ± 0.1 vs 2.3 ± 0.2, P<0.01). There were no other significant differences in the blood metabolites and hormones. In this small sample comparing subjects with metabolic disease with and without NAFLD, levels of ALT and the ratio of circulating unsaturated/saturated fatty acids are distinguishing features of NAFLD. These may be helpful measures to identify subjects with metabolic disease that require further evaluation for NAFLD.

scholarly journals Untargeted Metabolomics Analysis Revealed Lipometabolic Disorders in Perirenal Adipose Tissue of Rabbits Subject to a High-Fat Diet

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2289
Author(s):  
Siqi Xia ◽  
Jiahao Shao ◽  
Mauricio A. Elzo ◽  
Tao Tang ◽  
Yanhong Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Unsaturated Fatty Acids ◽  
High Resolution Mass Spectrometry ◽  
Untargeted Metabolomics ◽  
High Fat

A high-fat diet (HFD) is widely recognized as a significant modifiable risk for insulin resistance, inflammation, Type 2 diabetes, atherosclerosis and other metabolic diseases. However, the biological mechanism responsible for key metabolic disorders in the PAT of rabbits subject to HFD remains unclear. Here, untargeted metabolomics (LC-MS/MS) combined with liquid chromatography (LC) and high-resolution mass spectrometry (MS) were used to evaluate PAT metabolic changes. Histological observations showed that the adipocytes cells and density of PAT were significantly increased in HFD rabbits. Our study revealed 206 differential metabolites (21 up-regulated and 185 down-regulated); 47 differential metabolites (13 up-regulated and 34 down-regulated), comprising mainly phospholipids, fatty acids, steroid hormones and amino acids, were chosen as potential biomarkers to help explain metabolic disorders caused by HFD. These metabolites were mainly associated with the biosynthesis of unsaturated fatty acids, the arachidonic acid metabolic pathway, the ovarian steroidogenesis pathway, and the platelet activation pathway. Our study revealed that a HFD caused significant lipometabolic disorders. These metabolites may inhibit oxygen respiration by increasing the adipocytes cells and density, cause mitochondrial and endoplasmic reticulum dysfunction, produce inflammation, and finally lead to insulin resistance, thus increasing the risk of Type 2 diabetes, atherosclerosis, and other metabolic syndromes.

1734-P: High Dietary Fat Intake Exacerbates Insulin Resistance in a Type 2 Diabetes Genetic Mouse Model

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1734-P
Author(s):  
AUSTIN REILLY ◽  
SHIJUN YAN ◽  
ALEXA J. LONCHARICH ◽  
HONGXIA REN
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mouse Model ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Genetic Mouse Model

scholarly journals Visceral Adiposity Index is associated with Insulin Resistance, impaired Insulin Secretion, and β-cell dysfunction in subjects at risk for Type 2 Diabetes

2021 ◽  
pp. 100013
Author(s):  
Froylan David Martínez-Sánchez ◽  
Valerie Paola Vargas-Abonce ◽  
Andrea Rocha-Haro ◽  
Romina Flores-Cardenas ◽  
Milagros Fernández-Barrio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
At Risk ◽  
Insulin Secretion ◽  
Visceral Adiposity ◽  
Visceral Adiposity Index ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Impaired Insulin

scholarly journals Saturated Fatty Acids Promote GDF15 Expression in Human Macrophages through the PERK/eIF2/CHOP Signaling Pathway

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3771
Author(s):  
Laurent L’homme ◽  
Benan Pelin Sermikli ◽  
Bart Staels ◽  
Jacques Piette ◽  
Sylvie Legrand-Poels ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Er Stress ◽  
Signaling Pathway ◽  
Promoter Region ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Growth Differentiation Factor 15 ◽  
Human Macrophages ◽  
Primary Monocyte

Growth differentiation factor-15 (GDF-15) and its receptor GFRAL are both involved in the development of obesity and insulin resistance. Plasmatic GDF-15 level increases with obesity and is positively associated with disease progression. Despite macrophages have been recently suggested as a key source of GDF-15 in obesity, little is known about the regulation of GDF-15 in these cells. In the present work, we sought for potential pathophysiological activators of GDF15 expression in human macrophages and identified saturated fatty acids (SFAs) as strong inducers of GDF15 expression and secretion. SFAs increase GDF15 expression through the induction of an ER stress and the activation of the PERK/eIF2/CHOP signaling pathway in both PMA-differentiated THP-1 cells and in primary monocyte-derived macrophages. The transcription factor CHOP directly binds to the GDF15 promoter region and regulates GDF15 expression. Unlike SFAs, unsaturated fatty acids do not promote GDF15 expression and rather inhibit both SFA-induced GDF15 expression and ER stress. These results suggest that free fatty acids may be involved in the control of GDF-15 and provide new molecular insights about how diet and lipid metabolism may regulate the development of obesity and T2D.

scholarly journals Effects of dietary fat quantity and composition on fasting and postprandial levels of coagulation factor VII and serum choline-containing phospholipids

2003 ◽  
Vol 90 (2) ◽  
pp. 329-336 ◽  
Author(s):  
Anja Schou Lindman ◽  
Hanne Müller ◽  
Ingebjørg Seljeflot ◽  
Hans Prydz ◽  
Marit Veierød ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Coagulation Factor ◽  
Factor Vii ◽  
High Fat ◽  
Coagulation Factor Vii ◽  
Low Fat Diet

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisonsP≤0·01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0·001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisonsP≤0·05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0·03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0·001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.

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