Effects of dietary fat structure on short term changes in blood lipids and insulin sensitivity

Fermented soybean paste is an indigenous food for use in cooking in East and Southeast Asia. Korea developed and used its traditional fermented foods two thousand years ago. Chungkookjang has unique characteristics such as short-term fermentation (24–72 h) without salt, and fermentation mostly with Bacilli. Traditionally fermented chungkookjang (TFC) is whole cooked soybeans that are fermented predominantly by Bacillus species. However, Bacillus species are different in the environment according to the regions and seasons due to the specific bacteria. Bacillus species differently contribute to the bioactive components of chungkookjang, resulting in different functionalities. In this review, we evaluated the production process of poly-γ-glutamic acid (γ-PGA)-rich chungkookjang fermented with specific Bacillus species and their effects on memory function through the modulation of brain insulin resistance, neuroinflammation, and the gut–microbiome–brain axis. Bacillus species were isolated from the TFC made in Sunchang, Korea, and they included Bacillus (B.) subtilis, B. licheniformis, and B. amyloliquefaciens. Chungkookjang contains isoflavone aglycans, peptides, dietary fiber, γ-PGA, and Bacillus species. Chungkookjangs made with B. licheniformis and B. amyloliquefaciens have higher contents of γ-PGA, and they are more effective for improving glucose metabolism and memory function. Chungkookjang has better efficacy for reducing inflammation and oxidative stress than other fermented soy foods. Insulin sensitivity is improved, not only in systemic organs such as the liver and adipose tissues, but also in the brain. Chungkookjang intake prevents and alleviates memory impairment induced by Alzheimer’s disease and cerebral ischemia. This review suggests that the intake of chungkookjang (20–30 g/day) rich in γ-PGA acts as a synbiotic in humans and promotes memory function by suppressing brain insulin resistance and neuroinflammation and by modulating the gut–microbiome–brain axis.

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A common polymorphism near the interleukin-6 gene modifies the association between dietary fat intake and insulin sensitivity

Journal of Inflammation Research ◽

10.2147/jir.s27911 ◽

2012 ◽

pp. 1 ◽

Cited By ~ 1

Author(s):

Alaa Badawi ◽

Cuda ◽

Garcia-Bailo ◽

Karmali ◽

El-Sohemy

Keyword(s):

Insulin Sensitivity ◽

Dietary Fat ◽

Interleukin 6 ◽

Fat Intake ◽

Dietary Fat Intake ◽

Common Polymorphism

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Dietary fat and insulin sensitivity in a triethnic population: the role of obesity. The Insulin Resistance Atherosclerosis Study (IRAS)

American Journal of Clinical Nutrition ◽

10.1093/ajcn/65.1.79 ◽

1997 ◽

Vol 65 (1) ◽

pp. 79-87 ◽

Cited By ~ 125

Author(s):

E J Mayer-Davis ◽

J H Monaco ◽

H M Hoen ◽

S Carmichael ◽

M Z Vitolins ◽

...

Keyword(s):

Insulin Resistance ◽

Insulin Sensitivity ◽

Dietary Fat ◽

Insulin Resistance Atherosclerosis Study

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Insulin concentrations and insulin sensitivity after short-term amiloride in healthy subjects

European Journal of Clinical Pharmacology ◽

10.1007/bf00191913 ◽

1994 ◽

Vol 46 (5) ◽

Cited By ~ 4

Author(s):

J.W. Eriksson ◽

J. Fowelin ◽

V. Urbanavicius

Keyword(s):

Insulin Sensitivity ◽

Healthy Subjects ◽

Short Term

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OR28-6 Short-Term Mifepristone Treatment Improves Hepatic and Adipose Tissue Insulin Sensitivity in Overweight and Obese Subjects with Glucose Intolerance

Journal of the Endocrine Society ◽

10.1210/js.2019-or28-6 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Shivraj Grewal ◽

Susmeeta Sharma ◽

Raven McGlotten ◽

Ranganath Muniyappa ◽

Lynnette Nieman

Keyword(s):

Adipose Tissue ◽

Insulin Sensitivity ◽

Glucose Intolerance ◽

Short Term ◽

Obese Subjects

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Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

Journal of Endocrinology ◽

10.1530/joe-18-0567 ◽

2019 ◽

Vol 241 (1) ◽

pp. 59-70 ◽

Cited By ~ 8

Author(s):

Rodrigo Martins Pereira ◽

Kellen Cristina da Cruz Rodrigues ◽

Chadi Pellegrini Anaruma ◽

Marcella Ramos Sant’Ana ◽

Thaís Dantis Pereira de Campos ◽

...

Keyword(s):

Weight Loss ◽

Insulin Sensitivity ◽

Strength Training ◽

Term Strength ◽

Obese Mice ◽

Short Term ◽

Fat Accumulation ◽

Hepatic Insulin Sensitivity ◽

Short Term Strength ◽

Hepatic Fat

Non-alcoholic fatty liver disease (NAFLD) has a positive correlation with obesity, insulin resistance and type 2 diabetes mellitus (T2D). The aerobic training is an important tool in combating NAFLD. However, no studies have demonstrated the molecular effects of short-term strength training on the accumulation of hepatic fat in obese mice. This study aimed to investigate the effects of short-term strength training on the mechanisms of oxidation and lipid synthesis in the liver of obese mice. The short duration protocol was used to avoid changing the amount of adipose tissue. Swiss mice were separated into three groups: lean control (CTL), sedentary obese (OB) and strength training obese (STO). The obese groups were fed a high-fat diet (HFD) and the STO group performed the strength training protocol 1 session/day for 15 days. The short-term strength training reduced hepatic fat accumulation, increasing hepatic insulin sensitivity and controlling hepatic glucose production. The obese animals increased the mRNA of lipogenic genes Fasn and Scd1 and reduced the oxidative genes Cpt1a and Ppara. On the other hand, the STO group presented the opposite results. Finally, the obese animals presented higher levels of lipogenic proteins (ACC and FAS) and proinflammatory cytokines (TNF-α and IL-1β), but the short-term strength training was efficient in reducing this condition, regardless of body weight loss. In conclusion, there was a reduction of obesity-related hepatic lipogenesis and inflammation after short-term strength training, independent of weight loss, leading to improvements in hepatic insulin sensitivity and glycemic homeostasis in obese mice. Key points: (1) Short-term strength training (STST) reduced fat accumulation and inflammation in the liver; (2) Hepatic insulin sensitivity and HPG control were increased with STST; (3) The content and activity of ACC and content of FAS were reduced with STST; (4) STST improved hepatic fat accumulation and glycemic homeostasis; (5) STST effects were observed independently of body weight change.

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Inherent insulin sensitivity is a major determinant of multimeric adiponectin responsiveness to short-term weight loss in extreme obesity

Scientific Reports ◽

10.1038/srep05803 ◽

2014 ◽

Vol 4 (1) ◽

Cited By ~ 8

Author(s):

Stefania Mai ◽

Gillian E. Walker ◽

Amelia Brunani ◽

Gabriele Guzzaloni ◽

Glenda Grossi ◽

...

Keyword(s):

Weight Loss ◽

Insulin Sensitivity ◽

Major Determinant ◽

Extreme Obesity ◽

Short Term

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Role of TRIB3 in regulation of insulin sensitivity and nutrient metabolism during short-term fasting and nutrient excess

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00663.2011 ◽

2012 ◽

Vol 303 (7) ◽

pp. E908-E916 ◽

Cited By ~ 14

Author(s):

Jiarong Liu ◽

Wei Zhang ◽

Gin C. Chuang ◽

Helliner S. Hill ◽

Ling Tian ◽

...

Keyword(s):

Skeletal Muscle ◽

Oxygen Consumption ◽

Insulin Sensitivity ◽

Glucose Uptake ◽

Glucose Transport ◽

Oxygen Consumption Rate ◽

Glucose Oxidation ◽

Consumption Rate ◽

Negative Regulator ◽

Short Term

We have suggested previously that Tribbles homolog 3 (TRIB3), a negative regulator of Akt activity in insulin-sensitive tissues, could mediate glucose-induced insulin resistance in muscle under conditions of chronic hyperglycemia (Liu J, Wu X, Franklin JL, Messina JL, Hill HS, Moellering DR, Walton RG, Martin M, Garvey WT. Am J Physiol Endocrinol Metab 298: E565–E576, 2010). In the current study, we have assessed short-term physiological regulation of TRIB3 in skeletal muscle and adipose tissues by nutrient excess and fasting as well as TRIB3's ability to modulate glucose transport and mitochondrial oxidation. In Sprague-Dawley rats, we found that short-term fasting enhanced insulin sensitivity concomitantly with decrements in TRIB3 mRNA (66%, P < 0.05) and protein (81%, P < 0.05) in muscle and increments in TRIB3 mRNA (96%, P < 0.05) and protein (∼10-fold, P < 0.05) in adipose tissue compared with nonfasted controls. On the other hand, rats fed a Western diet for 7 days became insulin resistant concomitantly with increments in TRIB3 mRNA (155%, P < 0.05) and protein (69%, P = 0.0567) in muscle and a decrease in the mRNA (76%, P < 0.05) and protein (70%, P < 0.05) in adipose. In glucose transport and mitochondria oxidation studies using skeletal muscle cells, we found that stable TRIB3 overexpression impaired insulin-stimulated glucose uptake without affecting basal glucose transport and increased both basal glucose oxidation and the maximal uncoupled oxygen consumption rate. With stable knockdown of TRIB3, basal and insulin-stimulated glucose transport rates were increased, whereas basal glucose oxidation and the maximal uncoupled oxygen consumption rate were decreased. In conclusion, TRIB3 impacts glucose uptake and oxidation oppositely in muscle and fat according to levels of nutrient availability. The above data for the first time implicate TRIB3 as a potent physiological regulator of insulin sensitivity and mitochondrial glucose oxidation under conditions of nutrient deprivation and excess.

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