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Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3490
Author(s):  
Alice S. Ryan ◽  
Guoyan Li ◽  
Shawna McMillin ◽  
Steven J. Prior ◽  
Jacob B. Blumenthal ◽  
...  

Aging and obesity contribute to insulin resistance with skeletal muscle being critically important for maintaining whole-body glucose homeostasis. Both exercise and weight loss are lifestyle interventions that can affect glucose metabolism. The purpose of this study was to examine the effects of a six-month trial of aerobic exercise training or weight loss on signaling pathways in skeletal muscle in the basal condition and during hyperinsulinemia during a glucose clamp in middle-aged and older adults. Overweight and obese men and women aged 50–70 years were randomly allocated and completed six months of either weight loss (WL) (n = 18) or 3x/week aerobic exercise training (AEX) (n = 17). WL resulted in 10% weight loss and AEX increased maximal oxygen consumption (VO2max) (both p < 0.001). Insulin sensitivity (hyperinsulinemic-euglycemic 80 mU·m−2·min−1 clamp) increased in WL and AEX (both p < 0.01). In vivo insulin stimulation increased phosphorylation/total protein ratio (P/T) of protein kinase B (Akt), glycogen synthase kinase 3 beta (GSK-β3), 70 kDa ribosomal protein S6 kinase (p70S6k), insulin receptor substrate 1 (IRS-1), and insulin receptor (IR) expression (all p < 0.05) but not P/T extracellular regulated kinase ½ (ERK1/2), c-jun N-terminal kinases (JNK), p38 mitogen-activated protein kinases (p38), or insulin-like growth factor 1 receptor (IGF-1R). There were differences between WL and AEX in the change in basal Akt P/T (p = 0.05), GSK-3β P/T ratio (p < 0.01), p70S6k (p < 0.001), ERK1/2 (p = 0.01) P/T ratio but not p38, JNK, IRS-1, and IGF-1R P/T ratios. There was a difference between WL and AEX in the insulin stimulation changes in GSK3 which increased more after WL than AEX (p < 0.05). In the total group, changes in M were associated with changes in basal total GSK-3β and basal total p70Sk as well as insulin stimulation of total p70Sk. Protein signaling in skeletal muscle provides insight as to mechanisms for improvements in insulin sensitivity in aging and obesity.


2021 ◽  
Vol 8 ◽  
Author(s):  
Alice Glaves ◽  
Francisco Díaz-Castro ◽  
Javiera Farías ◽  
Rodrigo Ramírez-Romero ◽  
Jose E. Galgani ◽  
...  

Adipose tissue total amount, distribution, and phenotype influence metabolic health. This may be partially mediated by the metabolic effects that these adipose tissue characteristics exert on the nearby and distant tissues. Thus, adipose tissue may influence the capacity of cells, tissues, and the organism to adapt fuel oxidation to fuel availability, i.e., their metabolic flexibility (MetF). Our aim was to systematically review the evidence for an association between adipose tissue characteristics and MetF in response to metabolic challenges in human adults. We searched in PubMed (last search on September 4, 2021) for reports that measured adipose tissue characteristics (total amount, distribution, and phenotype) and MetF in response to metabolic challenges (as a change in respiratory quotient) in humans aged 18 to &lt;65 years. Any study design was considered, and the risk of bias was assessed with a checklist for randomized and non-randomized studies. From 880 records identified, 22 remained for the analysis, 10 of them measured MetF in response to glucose plus insulin stimulation, nine in response to dietary challenges, and four in response to other challenges. Our main findings were that: (a) MetF to glucose plus insulin stimulation seems inversely associated with adipose tissue total amount, waist circumference, and visceral adipose tissue; and (b) MetF to dietary challenges does not seem associated with adipose tissue total amount or distribution. In conclusion, evidence suggests that adipose tissue may directly or indirectly influence MetF to glucose plus insulin stimulation, an effect probably explained by skeletal muscle insulin sensitivity.Systematic Review Registration: PROSPERO [CRD42020167810].


2021 ◽  
Author(s):  
Kagabo Hirwa ◽  
Nishchil Patel ◽  
Abraham Biaye ◽  
Daniel Flanagan

2021 ◽  
Vol 4 (4) ◽  
pp. 01-04
Author(s):  
Aamir Jalal Al Mosawi

Dietary health supplements have increasingly used in the prevention and treatment of chronic disorders. During the previous decades, fenugreek (Trigonella foenum-graecum) seeds have been reported to have hypoglycemic and cholesterol lowering effects when used in type 1 and type 2 diabetes mellitus patients, and in experimental diabetic animals. The aim of this paper is to review fenugreek research findings relevant to its use in diabetes. There is convincing research evidence suggesting that fenugreek can improve hyperglycemia and has a protective effective against diabetic complications through immunomodulatory, insulin stimulation, and antioxidant effects, enhancing adipocyte differentiation, inhibition of inflammation in adipose tissues, and preventing or lessening pancreatic and renal damage. Many of the beneficial effects of fenugreek in diabetes have been attributed to four bioactive components including diosgenin, 4-hydroxyisoleucine, furostanolic saponins, and the fiber in fenugreek.


2021 ◽  
Vol 4 (4) ◽  
pp. 01-04
Author(s):  
Aamir Mosawi

Dietary health supplements have increasingly used in the prevention and treatment of chronic disorders. During the previous decades, fenugreek (Trigonella foenum-graecum) seeds have been reported to have hypoglycemic and cholesterol lowering effects when used in type 1 and type 2 diabetes mellitus patients, and in experimental diabetic animals. The aim of this paper is to review fenugreek research findings relevant to its use in diabetes. There is convincing research evidence suggesting that fenugreek can improve hyperglycemia and has a protective effective against diabetic complications through immunomodulatory, insulin stimulation, and antioxidant effects, enhancing adipocyte differentiation, inhibition of inflammation in adipose tissues, and preventing or lessening pancreatic and renal damage. Many of the beneficial effects of fenugreek in diabetes have been attributed to four bioactive components including diosgenin, 4-hydroxyisoleucine, furostanolic saponins, and the fiber in fenugreek.


2021 ◽  
Author(s):  
Brittany L. Dunkerly-Eyring ◽  
Miguel Pinilla-Vera ◽  
Desirae McKoy ◽  
Sumita Mishra ◽  
Maria Iziar Grajeda Martinez ◽  
...  

The mammalian target of rapamycin complex 1 (mTORC1) is tightly controlled by tuberous sclerosis complex-2 (TSC2), itself regulated by kinase phosphorylation reflecting environmental cues. Among these kinases is protein kinase G that modifies TSC2 at S1365 (S1364, human). This minimally affects basal mTORC1 activity, but upon phosphorylation or with an SE mutation, it blocks mTORC1 co-activation by pathological stress. An SA (phospho-silenced) mutation does the opposite. Here we reveal S1365 exerts biased regulation over mTORC1 activity (S6K phosphorylation). In myocytes and fibroblasts, ERK1/2 stimulated mTORC1 via endothelin-1 (ET-1) is potently and bidirectionally regulated by S1365. By contrast, Akt stimulation of mTORC1 (insulin) is minimally impacted. S1365 phosphorylation rises with ET-1 but not insulin stimulation, supporting intrinsic engagement by one and not the other. Energy and nutrient modulation of mTORC1 are minimally influenced by S1365. Consistent with these findings, knock-in mice with SA or SE mutations develop identical obesity, glucose intolerance, and fatty liver disease. These results reveal an ERK1/2-biased TSC2 regulatory mechanism controlling mTORC1 activation, with implications for suppressing pathological but not physiological mTORC1 stimulation.


Author(s):  
Brielle L. Dotson ◽  
Emily M. Heiston ◽  
Stephanie L. Miller ◽  
Steven K. Malin

Adults with metabolic syndrome (MetS) have increased fasting arterial stiffness and altered central hemodynamics that contribute, partly, to increased cardiovascular disease (CVD) risk. Although insulin affects aortic wave reflections in healthy adults, the effects in individuals with MetS are unclear. We hypothesized that insulin stimulation would reduce measures of pressure waveforms and hemodynamics in people with MetS. Thirty-five adults with obesity (27F; 54.2 ± 6.0 yr; 37.1 ± 4.8 kg/m2) were selected for MetS (ATP III criteria) following an overnight fast. Pulse wave analysis was assessed using applanation tonometry before and after a 2hr euglycemic-hyperinsulinemic clamp (90 mg/dl, 40 mU/m2/min). Deconvolution analysis was used to decompose the aortic waveform (augmentation index corrected to heart rate of 75 bpm (AIx@75); augmentation pressure (AP)) into backward and forward pressure components. Aerobic fitness (VO2max), body composition (DXA), and blood biochemistries were also assessed. Insulin significantly reduced augmentation index (AIx@75, 28.0 ± 9.6 vs. 23.0 ± 9.9 %, P<0.01), augmentation pressure (14.8 ± 6.4 vs. 12.0 ± 5.7 mmHg, P<0.01), pulse pressure amplification (1.26 ± 0.01 vs. 0.03 ± 0.01, P=0.01), and inflammation (hsCRP: P=0.02; MMP-7: P=0.03) compared to fasting. In subgroup analyses to understand HTN influence, there were no insulin stimulation differences on any outcome. VO2max, visceral fat, and blood potassium correlated with fasting AIx@75 (r=-0.39, P=0.02; r=0.41, P=0.03; r=-0.53, P=0.002). Potassium levels were also associated with insulin-mediated reductions in AP (r=0.52, P=0.002). Our results suggest insulin stimulation improves indices of aortic reflection in adults with MetS.


Author(s):  
Jaqueline K. Limberg ◽  
Rogerio Nogueira Soares ◽  
Gavin Power ◽  
Jennifer L. Harper ◽  
James A. Smith ◽  
...  

Herein we report in a sample of healthy young men (n=14) and women (n=12) that hyperinsulinemia induces time-dependent decreases in total peripheral resistance and its contribution to the maintenance of blood pressure. In the same participants, we observe profound vasodilatory effects of insulin in the lower limb despite concomitant activation of the sympathetic nervous system. We hypothesized this prominent peripheral vasodilation is possibly due to an ability of the leg vasculature to escape sympathetic vasoconstriction during systemic insulin stimulation. Consistent with this notion, we demonstrate in a subset of healthy men (n=9) and women (n=7) that systemic infusion of insulin blunts sympathetically-mediated leg vasoconstriction evoked by a cold pressor test, a well-established sympathoexcitatory stimulus. Further substantiating this observation, we show in mouse aortic rings that insulin exposure suppresses epinephrine and norepinephrine-induced vasoconstriction. Notably, we found that such insulin-suppressing effects on catecholamine-induced constriction are diminished following β-adrenergic receptor blockade. In accordance, we also reveal that insulin augments β-adrenergic-mediated vasodilation in isolated arteries. Collectively, these findings support the idea that sympathetic vasoconstriction can be attenuated during systemic hyperinsulinemia in the leg vasculature of both men and women and that this phenomenon may be in part mediated by potentiation of β-adrenergic vasodilation neutralizing α-adrenergic vasoconstriction.


2021 ◽  
Vol 478 (7) ◽  
pp. 1315-1319
Author(s):  
Luc Bertrand ◽  
Marine De Loof ◽  
Christophe Beauloye ◽  
Sandrine Horman ◽  
Laurent Bultot

Loss of the insulin-stimulated glucose uptake in muscle is a crucial event participating in the defect of whole-body metabolism in type 2 diabetes. Therefore, identification by Pavarotti et al. (Biochem. J (2021) 478 (2): 407–422) of complexin-2 as an important contributor to glucose transporter 4 (GLUT4) translocation to muscle cell plasma membrane upon insulin stimulation is essential. The present commentary discusses the biological importance of the findings and proposes future challenges and opportunities.


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