scholarly journals The effect of a short-term low-carbohydrate, high-fat diet with or without postmeal walks on glycemic control and inflammation in type 2 diabetes: a randomized trial

2018 ◽  
Vol 315 (6) ◽  
pp. R1210-R1219 ◽  
Author(s):  
Étienne Myette-Côté ◽  
Cody Durrer ◽  
Helena Neudorf ◽  
Tyler D. Bammert ◽  
José Diego Botezelli ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Cell Activation ◽  
Mononuclear Cells ◽  
Immune Cell ◽  
High Fat ◽  
Peripheral Blood Mononuclear ◽  
Time Interaction ◽  
Low Carbohydrate

Lowering carbohydrate consumption effectively lowers glucose, but impacts on inflammation are unclear. The objectives of this study were to: 1) determine whether reducing hyperglycemia by following a low-carbohydrate, high-fat (LC) diet could lower markers of innate immune cell activation in type 2 diabetes (T2D) and 2) examine if the combination of an LC diet with strategically timed postmeal walking was superior to an LC diet alone. Participants with T2D ( n = 11) completed a randomized crossover study involving three 4-day diet interventions: 1) low-fat low-glycemic index (GL), 2) and 3) LC with 15-min postmeal walks (LC+Ex). Four-day mean glucose was significantly lower in the LC+Ex group as compared with LC (−5%, P < 0.05), whereas both LC+Ex (−16%, P < 0.001) and LC (−12%, P < 0.001) conditions were lower than GL. A significant main effect of time was observed for peripheral blood mononuclear cells phosphorylated c-Jun N-terminal kinase ( P < 0.001), with decreases in all three conditions (GL: −32%, LC: −45%, and LC+Ex: −44%). A significant condition by time interaction was observed for monocyte microparticles ( P = 0.040) with a significant decrease in GL (−76%, P = 0.035) and a tendency for a reduction in LC (−70%, P = 0.064), whereas there was no significant change in LC+Ex (0.5%, P = 0.990). Both LC (−27%, P = 0.001) and LC+Ex (−35%, P = 0.005) also led to significant reductions in circulating proinsulin. An LC diet improved 4-day glycemic control and fasting proinsulin levels when compared with GL, with added glucose-lowering benefits when LC was combined with postmeal walking.

scholarly journals Deletion of GPR21 improves glucose homeostasis and inhibits the CCL2-CCR2 axis by divergent mechanisms

2021 ◽  
Vol 9 (2) ◽  
pp. e002285
Author(s):  
Darren M Riddy ◽  
Helene L Kammoun ◽  
Andrew J Murphy ◽  
Sanja Bosnyak-Gladovic ◽  
Rocio De la Fuente Gonzalez ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Homeostasis ◽  
Mononuclear Cells ◽  
Immune Cell ◽  
High Fat ◽  
Peripheral Blood Mononuclear ◽  
Monocyte Migration ◽  
Genotypic Analysis ◽  
Fat Feeding

IntroductionA potential role for the orphan G protein-coupled receptor, GPR21, in linking immune cell infiltration into tissues and obesity-induced insulin resistance has been proposed, although limited studies in mice are complicated by non-selective deletion of Gpr21.Research design and methodsWe hypothesized that a Gpr21-selective knockout mouse model, coupled with type 2 diabetes patient samples, would clarify these issues and enable clear assessment of GPR21 as a potential therapeutic target.ResultsHigh-fat feeding studies in Gpr21−/− mice revealed improved glucose tolerance and modest changes in inflammatory gene expression. Gpr21−/− monocytes and intraperitoneal macrophages had selectively impaired chemotactic responses to monocyte chemoattractant protein (MCP)-1, despite unaltered expression of Ccr2. Further genotypic analysis revealed that chemotactic impairment was due to dysregulated monocyte polarization. Patient samples revealed elevated GPR21 expression in peripheral blood mononuclear cells in type 2 diabetes, which was correlated with both %HbA1c and fasting plasma glucose levels.ConclusionsCollectively, human and mouse data suggest that GPR21 influences both glucose homeostasis and MCP-1/CCL2-CCR2-driven monocyte migration. However, a Gpr21−/− bone marrow transplantation and high-fat feeding study in mice revealed no effect on glucose homeostasis, suggesting that there is no (or limited) overlap in the mechanism involved for monocyte-driven inflammation and glucose homeostasis.

scholarly journals New Insights on the PBMCs Phospholipidome in Obesity Demonstrate Modulations Associated with Insulin Resistance and Glycemic Status

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3461
Author(s):  
Chloé Wilkin ◽  
Megan Colonval ◽  
Jonas Dehairs ◽  
Nathalie Esser ◽  
Margaud Iovino ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mononuclear Cells ◽  
Immune Cell ◽  
Negative Relationship ◽  
Peripheral Blood Mononuclear ◽  
Cell Dysfunction ◽  
Lipid Species ◽  
And Function

(1) Background: Obesity and type 2 diabetes have been suspected to impact both intrinsic metabolism and function of circulating immune cells. (2) Methods: To further investigate this immunometabolic modulation, we profiled the phospholipidome of the peripheral blood mononuclear cells (PBMCs) in lean, normoglycemic obese (OBNG) and obese with dysglycemia (OBDysG) individuals. (3) Results: The global PBMCs phospholipidome is significantly downmodulated in OBDysG unlike OBNG patients when compared to lean ones. Multiple linear regression analyses show a strong negative relationship between the global PBMCs phospholipidome and parameters assessing insulin resistance. Even though all classes of phospholipid are affected, the relative abundance of each class is maintained with the exception of Lyso-PC/PC and Lyso-PE/PE ratios that are downmodulated in PBMCs of OBDysG compared to OBNG individuals. Interestingly, the percentage of saturated PC is positively associated with glycated hemoglobin (HbA1c). Moreover, a few lipid species are significantly downmodulated in PBMCs of OBDysG compared to OBNG individuals, making possible to distinguish the two phenotypes. (4) Conclusions: This lipidomic study highlights for the first-time modulations of the PBMCs phospholipidome in obese patients with prediabetes and type 2 diabetes. Such phospholipidome remodeling could disrupt the cell membranes and the lipid mediator’s levels, driving an immune cell dysfunction.

scholarly journals Effects of the low carbohydrate, high fat diet on glycemic control and body weight in patients with type 2 diabetes: experience from a community-based cohort

2020 ◽  
Vol 8 (1) ◽  
pp. e000980 ◽  
Author(s):  
Shabina Roohi Ahmed ◽  
Sridevi Bellamkonda ◽  
Mihail Zilbermint ◽  
Jiangxia Wang ◽  
Rita Rastogi Kalyani
Keyword(s):  
Type 2 Diabetes ◽  
Body Weight ◽  
Glycemic Control ◽  
Usual Care ◽  
Care Group ◽  
High Fat ◽  
Community Based ◽  
Low Carbohydrate

ObjectiveThe optimal diet to improve glycemia in patients with type 2 diabetes remains unclear. Low carbohydrate, high fat (LCHF) diets can improve glycemic control, but have not been investigated in real-world settings.Research design and methodsWe investigated effects of the LCHF diet compared with usual care in a community-based cohort of patients with type 2 diabetes by performing a retrospective study of 49 patients who followed the LCHF diet for ≥3 months, and compared glycemic outcomes with age-matched and body mass index (BMI)-matched controls who received usual care (n=75). The primary outcome was change in A1C from baseline to the end of follow-up.ResultsCompared with the usual care group, the LCHF group showed a significantly greater reduction in A1C (−1.29% (95% CI −1.75 to −0.82; p<0.001)) and body weight (−12.8 kg (95% CI −14.7 to −10.8; p<0.001) at the end of follow-up after adjusting for age, sex, baseline A1C, BMI, baseline insulin dose. Of the patients initially taking insulin therapy in the LCHF group, 100% discontinued it or had a reduction in dose, compared with 23.1% in the usual care group (p<0.001). The LCHF group also had significantly greater reduction in fasting plasma glucose (−43.5 vs −8.5 mg/mL; p=0.03) compared with usual care.ConclusionsIn a community-based cohort of type 2 diabetes, the LCHF diet was associated with superior A1C reduction, greater weight loss and significantly more patients discontinuing or reducing antihyperglycemic therapies suggesting that the LCHF diet may be a metabolically favorable option in the dietary management of type 2 diabetes.

723-P: Effect of Low-Carbohydrate High-Fat vs. High-Carbohydrate Low-Fat Diet on HbA1c Control in Chinese Patients with Type 2 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 723-P
Author(s):  
LINGWANG AN ◽  
DANDAN WANG ◽  
XIAORONG SHI ◽  
CHENHUI LIU ◽  
KUEICHUN YEH ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Chinese Patients ◽  
High Fat ◽  
Low Fat ◽  
High Carbohydrate ◽  
Low Fat Diet ◽  
Low Carbohydrate ◽  
Hba1c Control

scholarly journals Endogenous retrovirus-encoded Syncytin-2 contributes to exosome-mediated immunosuppression of T cells†

2019 ◽  
Author(s):  
Adjimon G Lokossou ◽  
Caroline Toudic ◽  
Phuong Trang Nguyen ◽  
Xavier Elisseeff ◽  
Amandine Vargas ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell Activation ◽  
Map Kinases ◽  
Cell Activation ◽  
Mononuclear Cells ◽  
Immune Cell ◽  
Endogenous Retrovirus ◽  
Jurkat Cells ◽  
Peripheral Blood Mononuclear ◽  
Interfering Rna

Abstract Modulation of the activation status of immune cell populations during pregnancy depends on placental villous cytotrophoblast (VCT) cells and the syncytiotrophoblast (STB). Failure in the establishment of this immunoregulatory function leads to pregnancy complications. Our laboratory has been studying Syncytin-2 (Syn-2), an endogenous retroviral protein expressed in placenta and on the surface of placental exosomes. This protein plays an important role not only in STB formation through its fusogenic properties, but also through its immunosuppressive domain (ISD). Considering that Syn-2 expression is importantly reduced in preeclamptic placentas, we were interested in addressing its possible immunoregulatory effects on T cells. Activated Jurkat T cells and peripheral blood mononuclear cells (PBMCs) were treated with monomeric or dimerized version of a control or a Syn-2 ISD peptide. Change in phosphorylation levels of ERK1/2 MAP kinases was selectively noted in Jurkat cells treated with the dimerized ISD peptide. Upon incubation with the dimerized Syn-2 ISD peptide, significant reduction in Th1 cytokine production was further demonstrated by ELISA and Human Th1/Th2 Panel Multi-Analyte Flow Assay. To determine if exosome-associated Syn-2 could also be immunosuppressive placental exosomes were incubated with activated Jurkat and PBMCs. Quantification of Th1 cytokines in the supernatants revealed severe reduction in T cell activation. Interestingly, exosomes from Syn-2-silenced VCT incubated with PBMCs were less suppressive when compared with exosome derived from VCT transfected with control small interfering RNA (siRNA). Our results suggest that Syn-2 is an important immune regulator both locally and systemically, via its association with placental exosomes.

scholarly journals Increased Expression of Tissue Factor and Receptor for Advanced Glycation End Products in Peripheral Blood Mononuclear Cells of Patients With Type 2 Diabetes Mellitus with Vascular Complications

2004 ◽  
Vol 5 (2) ◽  
pp. 163-169 ◽  
Author(s):  
A. E. Buchs ◽  
A. Kornberg ◽  
M. Zahavi ◽  
D. Aharoni ◽  
C. Zarfati ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Advanced Glycation End Products ◽  
Mononuclear Cells ◽  
Vascular Complications ◽  
Advanced Glycation ◽  
Peripheral Blood Mononuclear ◽  
Glycation End Products ◽  
End Products ◽  
Blood Mononuclear Cells

The aim of the study was to determine the correlation between the expression of tissue factor (TF) and the receptor for advanced glycation end products (RAGEs) and vascular complications in patients with longstanding uncontrolled type 2 diabetes (T2D). TF and RAGE mRNAs as well as TF antigen and activity were investigated in 21 T2D patients with and without vascular complications. mRNA expression was assessed by reverse transcriptase–polymerase chain reaction (RT-PCR) in nonstimulated and advanced glycation end product (AGE) albumin–stimulated peripheral blood mononuclear cells (PBMCs). TF antigen expression was determined by enzyme-linked immunosorbent assay (ELISA) and TF activity by a modified prothrombin time assay. Basal RAGE mRNA expression was 0.2 ± 0.06 in patients with complications and 0.05 ± 0.06 patients without complications (P= .004). Stimulation did not cause any further increase in either group. TF mRNA was 0.58 ± 0.29 in patients with complications and 0.21 ± 0.18 in patients without complications (P= .003). Stimulation resulted in a nonsignificant increase in both groups. Basal TF activity (U/106PBMCs) was 18.4 ± 13.2 in patients with complications and 6.96 ± 5.2 in patients without complications (P= .003). It increased 3-fold in both groups after stimulation (P= .001). TF antigen (pg/106PBMCs) was 33.7 ± 28.6 in patients with complications, 10.4 ± 7.8 in patients without complications (P= .02). Stimulation tripled TF antigen in both groups of patients (P= .001). The RAGE/TF axis is up-regulated inT2Dpatients with vascular complications as compared to patients without complications. This suggests a role for this axis in the pathogenesis of vascular complications in T2D.

scholarly journals A Low-Carbohydrate/High-Fat Diet Improves Glucoregulation in Type 2 Diabetes Mellitus by Reducing Postabsorptive Glycogenolysis

2004 ◽  
Vol 89 (12) ◽  
pp. 6193-6197 ◽  
Author(s):  
Gideon Allick ◽  
Peter H. Bisschop ◽  
Mariette T. Ackermans ◽  
Erik Endert ◽  
Alfred J. Meijer ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
High Fat Diet ◽  
High Fat ◽  
Low Carbohydrate

Clinical significance of insulin peptide-specific interferon-γ-related immune responses in ketosis-prone type 2 diabetes

2021 ◽  
Author(s):  
Atsushi Satomura ◽  
Yoichi Oikawa ◽  
Akifumi Haisa ◽  
Seiya Suzuki ◽  
Shunpei Nakanishi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune Responses ◽  
Elispot Assay ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Β Cell ◽  
Peripheral Blood Mononuclear ◽  
Β Cell Function ◽  
Ifn Γ

Abstract Context Unprovoked A−β+ ketosis-prone type 2 diabetes (KPD) is characterized by the sudden onset of diabetic ketosis/ketoacidosis (DK/DKA) without precipitating factors, negative anti-islet autoantibodies (“A−”), and preservation of β-cell function (“β+”) after recovery from DKA. Although this phenotype often appears with acute hyperglycemia and DK/DKA just like acute-onset type 1 diabetes (AT1D), the involvement of anti-islet immune responses remains unknown. Objective We sought to clarify the immunological role of insulin-associated molecules in unprovoked A−β+ KPD. Methods In this cross-sectional study, blood samples from 75 participants (42 with AT1D and 33 with KPD) were evaluated for interferon (IFN)-γ-secreting peripheral blood mononuclear cells (PBMCs) reactive to four insulin B-chain amino acid 9–23-related peptides (B:9–23rPep) using an enzyme-linked immunospot (ELISpot) assay. Results Overall, 36.4% (12/33) of KPD participants showed positive IFN-γ ELISpot assay results; the positivity rate in KPD was similar to that in AT1D (38.1%; 16/42) and significantly higher than the previously reported rate in type 2 diabetes (8%; 2/25; P &lt; 0.0167). Moreover, B:9–23rPep-specific IFN-γ-producing PBMC frequency was negatively correlated with age and ad lib serum C-peptide levels in all KPD participants and positively correlated with HbA1c level in KPD participants with positive IFN-γ ELISpot results. Conclusions These findings suggest the involvement of B:9–23rPep-specific IFN-γ-related immunoreactivity in the pathophysiology of some unprovoked A−β+ KPD. Moreover, increased immunoreactivity may reflect transiently decreased β-cell function and increased disease activity at the onset of DK/DKA, thereby playing a key role in DK/DKA development in this KPD phenotype.

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