IGFBP5 suppresses oleate‐induced intramyocellular lipids deposition and enhances insulin signaling

2019 ◽  
Vol 234 (9) ◽  
pp. 15288-15298 ◽  
Author(s):  
Aoqi Xiang ◽  
Guiyan Chu ◽  
Youbo Zhu ◽  
Guangjun Ma ◽  
Gongshe Yang ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Intramyocellular Lipids

Short-term physical inactivity induces diacylglycerol accumulation and insulin resistance in muscle via lipin1 activation

2021 ◽  
Author(s):  
Saori Kakehi ◽  
Yoshifumi Tamura ◽  
Shin-ichi Ikeda ◽  
Naoko Kaga ◽  
Hikari Taka ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Physical Inactivity ◽  
Insulin Signaling Pathway ◽  
Dominant Negative ◽  
Short Term ◽  
Intramyocellular Lipids ◽  
Cast Immobilization ◽  
Impaired Insulin

Physical inactivity impairs muscle insulin sensitivity. However, its mechanism is unclear. To model physical inactivity, we applied 24-h hind-limb cast immobilization (HCI) to mice with normal or high fat diet (HFD), and evaluated intramyocellular lipids and the insulin signaling pathway in the soleus muscle. While 2-wk HFD alone did not alter intramyocellular diacylglycerol (IMDG) accumulation, HCI alone increased it by 1.9-fold and HCI after HFD further increased it by 3.3-fold. Parallel to this, we found increased PKCε activity, reduced insulin-induced 2-deoxy-glucose (2-DOG) uptake, and reduced phosphorylation of IRβ and Akt, key molecules for insulin signaling pathway. Lipin1, which converts phosphatidic acid to diacylglycerol, showed increase of its activity by HCI, and dominant-negative lipin1 expression in muscle prevented HCI-induced IMDG accumulation and impaired insulin-induced 2-DOG uptake. Further, 24-h leg cast immobilization in human increased lipin1 expression. Thus, even short-term immobilization increases IMDG and impairs insulin sensitivity in muscle via enhanced lipin1 activity.

Folate and vitamin B-12 deficiencies additively impaired memory function and disturbed the gut microbiota in amyloid-β infused rats

2019 ◽  
pp. 1-13 ◽  
Author(s):  
Sunmin Park ◽  
Sunna Kang ◽  
Da Sol Kim
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Insulin Signaling ◽  
Gut Microbiome ◽  
Metabolic Diseases ◽  
Memory Function ◽  
Amyloid Β ◽  
Impaired Memory ◽  
Ca1 Region ◽  
Folate And Vitamin B12

Abstract. Folate and vitamin B12(V-B12) deficiencies are associated with metabolic diseases that may impair memory function. We hypothesized that folate and V-B12 may differently alter mild cognitive impairment, glucose metabolism, and inflammation by modulating the gut microbiome in rats with Alzheimer’s disease (AD)-like dementia. The hypothesis was examined in hippocampal amyloid-β infused rats, and its mechanism was explored. Rats that received an amyloid-β(25–35) infusion into the CA1 region of the hippocampus were fed either control(2.5 mg folate plus 25 μg V-B12/kg diet; AD-CON, n = 10), no folate(0 folate plus 25 μg V-B12/kg diet; AD-FA, n = 10), no V-B12(2.5 mg folate plus 0 μg V-B12/kg diet; AD-V-B12, n = 10), or no folate plus no V-B12(0 mg folate plus 0 μg V-B12/kg diet; AD-FAB12, n = 10) in high-fat diets for 8 weeks. AD-FA and AD-VB12 exacerbated bone mineral loss in the lumbar spine and femur whereas AD-FA lowered lean body mass in the hip compared to AD-CON(P < 0.05). Only AD-FAB12 exacerbated memory impairment by 1.3 and 1.4 folds, respectively, as measured by passive avoidance and water maze tests, compared to AD-CON(P < 0.01). Hippocampal insulin signaling and neuroinflammation were attenuated in AD-CON compared to Non-AD-CON. AD-FAB12 impaired the signaling (pAkt→pGSK-3β) and serum TNF-α and IL-1β levels the most among all groups. AD-CON decreased glucose tolerance by increasing insulin resistance compared to Non-AD-CON. AD-VB12 and AD-FAB12 increased insulin resistance by 1.2 and 1.3 folds, respectively, compared to the AD-CON. AD-CON and Non-AD-CON had a separate communities of gut microbiota. The relative counts of Bacteroidia were lower and those of Clostridia were higher in AD-CON than Non-AD-CON. AD-FA, but not V-B12, separated the gut microbiome community compared to AD-CON and AD-VB12(P = 0.009). In conclusion, folate and B-12 deficiencies impaired memory function by impairing hippocampal insulin signaling and gut microbiota in AD rats.

Effects of weight loss combined with physical activity on intramyocellular lipids

2006 ◽  
Vol 1 (S 1) ◽  
Author(s):  
C Thamer ◽  
J Machann ◽  
A Niess ◽  
M Haap ◽  
C Claussen ◽  
...  
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Intramyocellular Lipids

Hypothalamic HSP10 Impacts Mitochondrial Dynamics, Insulin Signaling, and Liver Glycogen Content

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1801-P
Author(s):  
KRISTINA WARDELMANN ◽  
JOSÉ PEDRO CASTRO ◽  
MICHAELA RATH ◽  
JÜRGEN WEIß ◽  
ANNETTE SCHUERMANN ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Glycogen Content ◽  
Mitochondrial Dynamics ◽  
Liver Glycogen ◽  
Liver Glycogen Content

1806-P: Improvement Brain Insulin Signaling in Antidiabetic Effect of Duodenal Jejunal Bypass Surgery

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1806-P ◽  
Author(s):  
QINGTAO YAN ◽  
NA LI ◽  
RUIYAN PAN ◽  
HUAI-JIE WANG ◽  
BIN JIANG ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Bypass Surgery ◽  
Antidiabetic Effect ◽  
Brain Insulin ◽  
Jejunal Bypass

1714-P: Regulation of Phosphorylation Status in Insulin Signaling via a4 Is Necessary for Adipocyte Maintenance and Lipid Dynamics

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1714-P
Author(s):  
MASAJI SAKAGUCHI ◽  
SHOTA OKAGAWA ◽  
YUMA OKUBO ◽  
SAYAKA KITANO ◽  
MOTOYUKI IGATA ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Lipid Dynamics

Possibility of distinct insulin-signaling pathways beyond phosphatidylinositol 3-kinase-mediating glucose transport and lipogenesis

Diabetes ◽  
1998 ◽  
Vol 47 (2) ◽  
pp. 179-185 ◽  
Author(s):  
R. W. Stevenson ◽  
D. K. Kreutter ◽  
K. M. Andrews ◽  
P. E. Genereux ◽  
E. M. Gibbs
Keyword(s):  
Signaling Pathways ◽  
Glucose Transport ◽  
Insulin Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

High-fat feeding impairs insulin-stimulated GLUT4 recruitment via an early insulin-signaling defect

Diabetes ◽  
1997 ◽  
Vol 46 (2) ◽  
pp. 215-223 ◽  
Author(s):  
J. R. Zierath ◽  
K. L. Houseknecht ◽  
L. Gnudi ◽  
B. B. Kahn
Keyword(s):  
Insulin Signaling ◽  
High Fat ◽  
Fat Feeding
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