scholarly journals Long-term dysbiosis promotes insulin resistance during obesity despite rapid diet-induced changes in the gut microbiome of mice

2017 ◽  
Author(s):  
Kevin P. Foley ◽  
Emmanuel Denou ◽  
Brittany M. Duggan ◽  
Rebecca Chan ◽  
Jennifer C. Stearns ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Intestinal Microbiota ◽  
Fecal Microbiota ◽  
Taxonomic Composition ◽  
Short Term ◽  
Fecal Microbiome ◽  
Induced Changes

AbstractThe intestinal microbiota and insulin sensitivity are rapidly altered in response to a high fat diet (HFD). It is unclear if gut dysbiosis precedes insulin resistance or vice versa. The initial triggers of diet-induced insulin resistance can differ from mechanisms underlying chronic dysglycemia during prolonged obesity. It is not clear if intestinal dysbiosis contributes to insulin resistance during short-term or long-term HFD-feeding. We found that diet-induced changes in the composition of the fecal microbiome preceded changes in glucose and insulin tolerance at both the onset and removal of a HFD in mice. Dysbiosis occurred after 1-3 days of HFD-feeding, whereas insulin and glucose intolerance manifested by 3-4 days. Antibiotic treatment did not alter glucose tolerance during this short-term HFD period. Conversely, antibiotics improved glucose tolerance in mice with protracted obesity caused by long-term HFD feeding for over 2 months. We also found that microbiota transmissible glucose intolerance only occurred after prolonged diet-induced dysbiosis. Germ-free mice had impaired glucose tolerance when reconstituted with the microbiota from long-term, but not short-term HFD-fed animals. Our results are consistent with intestinal microbiota contributing to chronic insulin resistance and dysglycemia during prolonged obesity, despite rapid diet-induced changes in the taxonomic composition of the fecal microbiota.

Insulin resistance caused by amylin in conscious rats is independent of induced hypocalcemia and fades during long-term exposure

1993 ◽  
Vol 129 (4) ◽  
pp. 360-365 ◽  
Author(s):  
Clemens Fürnsinn ◽  
Peter Nowotny ◽  
Michael Roden ◽  
Madeleine Rohac ◽  
Thomas Pieber ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Tolerance Test ◽  
Zucker Rats ◽  
Control Group ◽  
Short Term ◽  
Euglycemic Hyperinsulinemic Clamp

To compare the effect of short- vs long-term amylin infusion on insulin sensitivity, glucose tolerance and serum calcemia, euglycemic-hyperinsulinemic clamp (26 pmol·kg−1·min−1) and glucose tolerance tests (2.4 mmol/kg over 30 min) were performed in lean Zucker rats. Three infusion protocols were employed: control group: 24 h of iv saline; short-term amylin exposure: 22 h of iv saline followed by 2 h of iv amylin (20 μg/h); long-term amylin exposure: 24 h of iv amylin (20 μg/h). Insulin resistance was induced by short-term amylin infusion during euglycemic clamping, as shown by a 41% decrease in space-corrected glucose infusion rates (μmol·kg−1·min−1; control group, 106.0±15.0; short-term iv amylin, 62.7±15.0; p<0.00 5). After long-term amylin exposure, insulin sensitivity was identical to control values (109.9±6.7). This fading action of amylin was confirmed by data from the glucose tolerance test, demonstrating glucose intolerance after short- but not after long-term amylin exposure. Serum calcium concentration decreased during short-term (2 h) amylin infusion (from 2.52±0.15 to 2.09±0.12 mmol/l; p<0.01) and hypocalcemia of a similar extent also was present after 22 h and 24 h of amylin exposure (2.10±0.09 and 2.04±0.14 mmol/l, respectively). The data demonstrate that short-term amylin infusion induces insulin resistance and glucose intolerance, both of which vanish during long-term (>22 h) amylin exposure, being apparently independent of induced hypocalcemia.

scholarly journals Effect of stevia on the gut microbiota and glucose tolerance in a murine model of diet-induced obesity

2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Treatment Groups ◽  
Low Fat Diet ◽  
Taxonomic Groups ◽  
Induced Changes

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.

scholarly journals The Effect of Pesticides on the Microbiome of Animals

Agriculture ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 79 ◽  
Author(s):  
Mikhail Y. Syromyatnikov ◽  
Mariya M. Isuwa ◽  
Olga V. Savinkova ◽  
Mariya I. Derevshchikova ◽  
Vasily N. Popov
Keyword(s):  
Intestinal Microbiota ◽  
Mating Success ◽  
Taxonomic Composition ◽  
Scientific Data ◽  
Negative Effects ◽  
Negative Effect ◽  
Bacterial Biodiversity ◽  
Induced Changes ◽  
The Impact ◽  
Impact Of Pesticides

In recent decades an increase in the use of pesticides to protect plants from pests, diseases and weeds has been observed. There are many studies on the effects of various pesticides on non-target organisms. This review aims to analyze and summarize published scientific data on the effects of pesticides on the animal microbiome. Pesticides can affect various parameters of the animal microbiome, such as the taxonomic composition of bacteria, bacterial biodiversity, and bacterial ratios and modify the microbiome of various organisms from insects to mammals. Pesticide induced changes in the microbiome reducing the animal’s immunity. The negative effects of pesticides could pose a global problem for pollinators. Another possible negative effect of pesticides is the impact of pesticides on the intestinal microbiota of bumblebees and bees that increase the body’s sensitivity to pathogenic microflora, which leads to the death of insects. In addition, pesticides can affect vitality, mating success and characteristics of offspring. The review considers methods for correcting of bee microbiome.

scholarly journals Saturated- and n-6 Polyunsaturated-Fat Diets Each Induce Ceramide Accumulation in Mouse Skeletal Muscle: Reversal and Improvement of Glucose Tolerance by Lipid Metabolism Inhibitors

Endocrinology ◽  
2010 ◽  
Vol 151 (9) ◽  
pp. 4187-4196 ◽  
Author(s):  
G. Frangioudakis ◽  
J. Garrard ◽  
K. Raddatz ◽  
J. L. Nadler ◽  
T. W. Mitchell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
De Novo ◽  
Saturated Fat ◽  
Tolerance Test ◽  
Polyunsaturated Fat ◽  
Unsaturated Fat ◽  
Fat Diets

Lipid-induced insulin resistance is associated with intracellular accumulation of inhibitory intermediates depending on the prevalent fatty acid (FA) species. In cultured myotubes, ceramide and phosphatidic acid (PA) mediate the effects of the saturated FA palmitate and the unsaturated FA linoleate, respectively. We hypothesized that myriocin (MYR), an inhibitor of de novo ceramide synthesis, would protect against glucose intolerance in saturated fat-fed mice, while lisofylline (LSF), a functional inhibitor of PA synthesis, would protect unsaturated fat-fed mice. Mice were fed diets enriched in saturated fat, n-6 polyunsaturated fat, or chow for 6 wk. Saline, LSF (25 mg/kg · d), or MYR (0.3 mg/kg · d) were administered by mini-pumps in the final 4 wk. Glucose homeostasis was examined by glucose tolerance test. Muscle ceramide and PA were analyzed by mass spectrometry. Expression of LASS isoforms (ceramide synthases) was evaluated by immunoblotting. Both saturated and polyunsaturated fat diets increased muscle ceramide and induced glucose intolerance. MYR and LSF reduced ceramide levels in saturated and unsaturated fat-fed mice. Both inhibitors also improved glucose tolerance in unsaturated fat-fed mice, but only LSF was effective in saturated fat-fed mice. The discrepancy between ceramide and glucose tolerance suggests these improvements may not be related directly to changes in muscle ceramide and may involve other insulin-responsive tissues. Changes in the expression of LASS1 were, however, inversely correlated with alterations in glucose tolerance. The demonstration that LSF can ameliorate glucose intolerance in vivo independent of the dietary FA type indicates it may be a novel intervention for the treatment of insulin resistance.

scholarly journals Drug-Induced Changes in Risk/Biomarkers and Their Relationship with Renal and Cardiovascular Long-Term Outcome in Patients with Diabetes

2011 ◽  
Vol 57 (2) ◽  
pp. 186-195 ◽  
Author(s):  
Yan Miao ◽  
Paul A Smink ◽  
Dick de Zeeuw ◽  
Hiddo J Lambers Heerspink
Keyword(s):  
Risk Management ◽  
Short Term ◽  
Drug Induced ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Patients With Diabetes ◽  
Changes In Risk ◽  
Risk Biomarkers ◽  
Induced Changes

BACKGROUND Optimal renal and cardiovascular risk management in diabetic patients includes optimal maintenance of blood pressure and control of glucose and lipids. Although the optimal control of these risk factors or “risk/biomarkers” has proven to be effective, it often is difficult to achieve. Consequently, the risk for renal and cardiovascular complications remains devastatingly high. Many risk/biomarkers have been discovered that accurately predict long-term renal and cardiovascular outcome. However, the aim of measuring risk/biomarkers may not be only to determine an individual's risk, but also to use the risk/biomarker level to guide therapy and thereby improve long-term clinical outcome. CONTENT This review describes the effects of various drugs on novel risk/biomarkers and the relationship between (drug induced) short-term changes in risk/biomarkers and long-term renal and cardiovascular outcome in patients with diabetes. SUMMARY In post hoc analyses of large trials, the short-term reductions in albuminuria, transforming growth factor-β, and N-terminal pro-B–type natriuretic peptide (NT-proBNP) induced by inhibitors of the renin-angiotensin-aldosterone system were associated with a decreased likelihood of long-term adverse renal and cardiovascular outcomes. However, the few studies that systematically investigated the utility of prospectively targeting novel risk/biomarkers such as hemoglobin or NT-proBNP failed to demonstrate long-term cardiovascular protection. The latter examples suggest that although a risk/biomarker may have superior prognostic ability, therapeutically changing such a risk/biomarker does not necessarily improve long-term outcome. Thus, to establish the clinical utility of other novel risk/biomarkers, clinical trials must be performed to prospectively examine the effects of therapeutically-induced changes in single or multiple risk/biomarkers on long-term risk management of patients with diabetes.

scholarly journals Glucose Intolerance, Insulin Resistance, and Hyperandrogenemia in First Degree Relatives of Women with Polycystic Ovary Syndrome

2003 ◽  
Vol 88 (5) ◽  
pp. 2031-2036 ◽  
Author(s):  
Bülent O. Yildiz ◽  
Hakan Yarali ◽  
Havva Oguz ◽  
Miyase Bayraktar
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Matched Control ◽  
Polycystic Ovary ◽  
Family Members ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Ovary Syndrome ◽  
First Degree Relatives

Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [MothersPCOS (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m2), FathersPCOS (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m2), SistersPCOS (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m2), and BrothersPCOS (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m2)] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. ControlMothersPCOS, ControlFathersPCOS, ControlSistersPCOS, and ControlBrothersPCOS) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUCinsulin) in NGT MothersPCOS, FathersPCOS, SistersPCOS, BrothersPCOS, and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of MothersPCOS and 27% and 31% of FathersPCOS, respectively. There was no diabetes in SistersPCOS and BrothersPCOS. IGT was found in 5% of SistersPCOS. Impaired fasting glucose was found in 3% of MothersPCOS and 4% of BrothersPCOS. The analysis of NGT family members showed that MothersPCOS had higher FI (P &lt; 0.05), HOMA IR (P &lt; 0.05), and AUCinsulin (P &lt; 0.01) and lower FGI (P &lt; 0.05) than ControlMothersPCOS, whereas all IR parameters were comparable between FathersPCOS and their matched control subgroup. SistersPCOS had higher FI (P &lt; 0.05), HOMA IR (P &lt; 0.01), and AUCinsulin (P &lt; 0.05) and lower FGI (P &lt; 0.01), and BrothersPCOS had higher AUCinsulin (P &lt; 0.01) than their matched control subgroups, respectively. MothersPCOS had higher testosterone levels than ControlMothersPCOS (P &lt; 0.01 and P &lt; 0.05 for pre- and postmenopausal women, respectively). SistersPCOS had higher LH (P &lt; 0.01), testosterone (P &lt; 0.001), androstenedione (P &lt; 0.01), and dehydroepiandrosterone sulfate (P &lt; 0.05) levels than ControlSistersPCOS. There was no difference in gonadotropin and androgen levels in FathersPCOS compared with ControlFathersPCOS or in BrothersPCOS compared with ControlBrothersPCOS. Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.

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