Relationship of insulin resistance and glucose to tau PET positivity

Current studies show that metabolic and behavioral disorders represent severe health problems. Several questions arise about the molecular relationship of metabolic and behavioral disorders. This review will discuss the relationship of lipid metabolism and fructose consumption accompanied by an increase in weight as well as associated disorders: hypertension, insulin-resistance, oxidative stress and depression. Adipose tissue is considered as an endocrine tissue with intense secretory activities (metabolic and inflammatory). These adipokines are responsible for an alteration of several physiological functions. In this review we will try to understand how lipogenesis that causes dyslipidemia can influence insulin resistance, hypertension, oxidative stress, depression and the relationship between these various disorders.

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BCAA Supplementation in Mice with Diet-Induced Obesity Alters the Metabolome Without Impairing Glucose Homeostasis

Endocrinology ◽

10.1210/endocr/bqab062 ◽

2021 ◽

Author(s):

Jennifer Lee ◽

Archana Vijayakumar ◽

Phillip J White ◽

Yuping Xu ◽

Olga Ilkayeva ◽

...

Keyword(s):

Insulin Resistance ◽

Glucose Homeostasis ◽

Obese Mice ◽

High Fat ◽

Leucine Oxidation ◽

Insulin Resistant ◽

Diet Induced Obesity ◽

Chain Acyl ◽

Branched Chain ◽

Relationship Of

Abstract Circulating branched chain amino acid (BCAA) levels are elevated in obese humans and genetically obese rodents. However, the relationship of BCAAs to insulin resistance in diet-induced obese mice, a commonly used model to study glucose homeostasis, is still ill-defined. Here we examined how high-fat high-sucrose (HFHS) or high-fat diet (HFD) feeding, with or without BCAA supplementation in water, alters the metabolome in serum/plasma and tissues in mice and whether raising circulating BCAA levels worsens insulin resistance and glucose intolerance. Neither HFHS nor HFD-feeding raised circulating BCAA levels in insulin-resistant diet-induced obese mice. BCAA supplementation raised circulating BCAA and BCKA levels and C5-OH/C3-DC acylcarnitines (AC) in muscle from HFHS or HFD-fed mice, but did not worsen insulin resistance. A set of short and long-chain acyl CoAs were elevated by diet alone in muscle, liver and WAT, but not increased further by BCAA supplementation. HFD feeding reduced valine and leucine oxidation in WAT but not in muscle. BCAA supplementation markedly increased valine oxidation in muscle from HFD-fed mice while leucine oxidation was unaffected by diet or BCAA treatment. Here we establish an extensive metabolome database showing tissue-specific changes in mice on two different HFDs, with or without BCAA supplementation. We conclude that mildly elevating circulating BCAAs and a subset of ACs by BCAA supplementation does not worsen insulin resistance or glucose tolerance in mice. This work highlights major differences in the effects of BCAAs on glucose homeostasis in diet-induced obese mice versus data reported in obese rats and in humans.

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Circulating Apolipoprotein L1 is associated with insulin resistance-induced abnormal lipid metabolism

Scientific Reports ◽

10.1038/s41598-019-51367-7 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 1

Author(s):

Kenji Nishimura ◽

Taichi Murakami ◽

Toshihiro Sakurai ◽

Masashi Miyoshi ◽

Kiyoe Kurahashi ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Density Lipoprotein ◽

Hdl Cholesterol ◽

Insulin Resistant ◽

Cell Dysfunction ◽

Fractionation Analysis ◽

Abnormal Lipid Metabolism ◽

Hdl Metabolism ◽

Relationship Of

Abstract Circulating ApolipoproteinL1 (ApoL1) is a component of pre-β-high-density lipoprotein (HDL), however little is known about the relationship of ApoL1 with cardiometabolic factors. Considering previous studies reporting the correlation of ApoL1 to triglyceride, we have hypothesized that ApoL1 associates with insulin-related metabolism. The current study examined their associations in 126 non-diabetic subjects and 36 patients with type 2 diabetes (T2DM). Non-diabetic subjects demonstrated triglyceride (standardized coefficients [s.c.] = 0.204, p < 0.05), body mass index (s.c. =0.232, p < 0.05) and HDL cholesterol (s.c. = −0.203, p < 0.05) as independent determinant of ApoL1 levels, and the significant elevation of ApoL1 in metabolic syndrome. Lipoprotein fractionation analysis revealed the predominant distribution of ApoL1 in large HDL fraction, and the significant increase of ApoL1 in large LDL fraction in high ApoL1 samples with insulin resistance. In T2DM, ApoL1 was higher in T2DM with metabolic syndrome, however ApoL1 was lower with β cell dysfunction. Insulin significantly promotes ApoL1 synthesis and secretion in HepG2 cells. In conclusion, circulating ApoL1 may be associated with abnormal HDL metabolism in insulin resistant status. This may suggest a regulation of insulin signal on the ApoL1 level, leading to offer a novel insight to the ApoL1 biology.

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