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How to ACTUALLY Lose Belly Fat (Based on Science) An excess of visceral Visceral fat and nutrient metabolism can, therefore, have Viscearl dangerous consequences. Energize and Restore visceral fat is Viscwral the abdominal Visceral fat and nutrient metabolism, it is close to many vital organs, such as the Visderal, liver, and intestines. The higher the Visceral fat and nutrient metabolism of visceral fat nugrient person stores, Viscerao more at risk they nutruent for certain health complications, such as type 2 diabetes and heart disease. Imaging scans, such as computed tomography CT or magnetic resonance imaging MRI scans are the most accurate way to determine whether someone has visceral fat. However, because conducting these scans is both expensive and time-consuming, a doctor is more likely to diagnose visceral fat by asking a person questions about their diet and lifestyle. Another useful way to determine how much visceral fat a person is carrying is to measure the size of their waist. A woman whose waist measures 35 inches or more is likely to have excess visceral fat.Visceral fat and nutrient metabolism -
Intermittent fasting is a popular way to lose weight. Unlike dieting, intermittent fasting does not restrict any foods. It simply focuses on when you should eat them. Following an intermittent style of eating will generally make you eat fewer meals and, in turn, fewer calories.
Studies also show that intermittent fasting may help you lose visceral fat 76 , You can find out more about intermittent fasting and how to do it here.
Visceral fat is incredibly harmful and may increase your risk of chronic disease, including heart disease, type 2 diabetes and even certain cancers.
Some of these include eating fewer carbs and less added sugar, doing more aerobic exercise and increasing your protein intake. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.
We all have belly fat, but having too much can harm your health. This article explains the different types of belly fat, how they affect your health…. Visceral fat is located near vital organs like the liver and stomach.
Find out about diagnosis, the complications it may cause, and more. Everyone is born with subcutaneous fat. It can indicate risk for…. Patients with diabetes who used GLP-1 drugs, including tirzepatide, semaglutide, dulaglutide, and exenatide had a decreased chance of being diagnosed….
Some studies suggest vaping may help manage your weight, but others show mixed…. The amount of time it takes to recover from weight loss surgery depends on the type of surgery and surgical technique you receive.
New research suggests that running may not aid much with weight loss, but it can help you keep from gaining weight as you age. Here's why. New research finds that bariatric surgery is an effective long-term treatment to help control high blood pressure.
Most people associate stretch marks with weight gain, but you can also develop stretch marks from rapid weight loss. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based How to Get Rid of Visceral Fat.
By Ryan Raman, MS, RD — Updated on April 12, What Is Visceral Fat? Share on Pinterest. Why Is Visceral Fat Harmful? Try a Low-Carb Diet. Do More Aerobic Exercise.
Try Eating More Soluble Fiber. Eat More Protein. Limit Added Sugar Intake. Limit Alcohol Intake. Avoid Trans Fat. Get Plenty of Sleep. Reduce Your Stress Levels. Try a Probiotic. Try Intermittent Fasting. The Bottom Line. How we reviewed this article: History. Apr 12, Written By Ryan Raman.
Share this article. Read this next. The 2 Types of Belly Fat and How to Lose It. By Jillian Kubala, MS, RD. Visceral Fat. Medically reviewed by Danielle Hildreth, RN, CPT. What Is Subcutaneous Fat? Medically reviewed by Judith Marcin, M. GLP-1 Drugs Like Ozempic and Mounjaro Linked to Lower Risk of Depression Patients with diabetes who used GLP-1 drugs, including tirzepatide, semaglutide, dulaglutide, and exenatide had a decreased chance of being diagnosed… READ MORE.
Does Vaping Make You Lose Weight? How Long Does It Take to Recover from Weight Loss Surgery? Amalia Gastaldelli, Yoshinori Miyazaki, Maura Pettiti, Masafumi Matsuda, Srihanth Mahankali, Eleonora Santini, Ralph A.
Visceral fat VF excess has been associated with decreased peripheral insulin sensitivity and has been suggested to contribute to hepatic insulin resistance.
However, the mechanisms by which VF impacts on hepatic glucose metabolism and the quantitative role of VF in glycemic control have not been investigated.
In the present study 63 type 2 diabetic subjects age, 55 ± 1 yr; fasting plasma glucose, 5. In contrast, the relation of basal endogenous glucose output to VF was not statistically significant.
We conclude that in patients with established type 2 diabetes, VF accumulation has a significant negative impact on glycemic control through a decrease in peripheral insulin sensitivity and an enhancement of gluconeogenesis.
We 8 and others 9 have reported that gluconeogenesis GNG is enhanced in type 2 diabetic patients, and that insulin is less potent in suppressing GNG than glycogenolysis GLY 10 , Several lines of evidence have suggested a role for visceral fat VF accumulation in the pathogenesis of insulin resistance.
Thus, VF excess has been associated with 1 decreased sensitivity of glucose uptake to insulin stimulation as measured by the euglycemic insulin clamp technique 12 , 2 reduced rate of free fatty acids FFA reesterification 13 , and 3 increased resistance of lipolysis to the inhibitory effect of insulin in both visceral and peripheral adipocytes 14 , It has been postulated that preferential influx of FFA and other molecules produced by visceral adipocytes via the portal circulation into the liver can induce or augment hepatic insulin resistance, in particular by enhancing GNG.
However, direct evidence bearing on such hepatic effects is not, to our knowledge, available, nor is it clear whether such putative effects are great enough to influence fasting hyperglycemia and overall glycemic control in diabetic patients. In addition, VF accumulation is strongly related to overall adiposity 16 , and this makes it mandatory to account for obesity when attempting to establish an independent role for VF in metabolic control.
The present study was undertaken to explore the relationship between VF [quantitated by magnetic resonance imaging MRI ] and the severity of fasting hyperglycemia in a large group of type 2 patients, independently of confounders such as sex, age, and obesity.
We also examined potential mechanisms insulin-mediated glucose disposal, endogenous glucose output, GNG, and GLY underlying such a relationship by employing the insulin clamp technique in combination with tracers. The present series included 63 subjects with type 2 diabetes 37 Mexican-Americans and 26 Caucasians with a wide range of FPG 5.
None of the patients was treated with insulin, metformin, or thiazolidinediones. Subjects were not taking any other drugs known to affect glucose tolerance. The study protocol was approved by the institutional review board of the University of Texas Health Science Center, and informed written consent was obtained from each subject before participation.
Within a 5- to 7-d interval, all subjects received 1 measurement of fat-free mass FFM with the use of an iv bolus of 3 H 2 O, 2 quantitation of sc and intraabdominal VF content using MRI, and 3 a euglycemic hyperinsulinemic clamp to measure insulin sensitivity combined with a primed-constant infusion of [3- 3 H]glucose for measurement of EGO and 2 H 2 O ingestion in 48 of the 63 study subjects to measure the contribution of GNG and GLY to EGO.
On the day of the study subjects were admitted to the Clinical Research Center at h. Height and weight were recorded, arterial blood pressure was measured, and waist and hip circumferences were measured to the nearest centimeter.
A catheter was placed into an antecubital vein, and subjects received a μCi iv bolus of 3 H 2 O. Blood samples were drawn at 90, , and min for the determination of plasma 3 H 2 O radioactivity.
FFM was calculated as described previously 17 , and fat mass was determined as the difference between body weight and FFM. Intraabdominal VF and sc fat SF depots were measured by MRI, using imaging procedures previously described Briefly, images were acquired on a 1.
A sagittal localizing image was used to center transverse sections on the line through the space between L4 and L5. Ten 5. The field of view ranged from 30—50 cm depending on body size. Phase encoding was in the antero-posterior direction to minimize the effects of motion-induced phase artifacts that might otherwise be distributed laterally through a large portion of the abdomen.
The field of view was adjusted for body size to ensure a 2-mm pixel spacing. Signal averaging four-signal average was used to reduce the effect of motion-related artifacts. Additionally, respiratory gating was used to combat motion-induced artifacts and to reduce the blurring of fat boundaries in the anterior region of the abdomen.
Images were processed using Alice Software Perceptive Systems, Inc. The SF area was analyzed by selecting the outer and inner margins of sc adipose tissue as the region of interest from the cross-sectional images and counting the number of pixels between the outer and inner margins of sc adipose tissue.
The visceral intraabdominal fat area was determined using histograms specific to the visceral regions. The histograms were summed over the range of pixel values designated as fat by fitting two normal analysis distribution curves to them.
In the morning on the day before the study, a blood sample for the determination of background 2 H 2 O enrichment was taken. The following morning, subjects were admitted to the Clinical Research Center at h after a h overnight fast.
A polyethylene cannula was inserted into an antecubital vein for the infusion of all test substances. A second catheter was inserted retrogradely into an ipsilateral wrist vein on the dorsum of the hand for blood sampling, and the hand was kept in a heated box at 65 C. A primed μCi -constant infusion of 3-[ 3 H]glucose NEN Life Science Products, Boston, MA was started at h and continued at a rate of 0.
During the last 30 min of the basal equilibration period — min after the start of 3-[ 3 H]glucose , plasma samples were taken at 5- to min intervals for the determination of plasma glucose, FFA, and insulin concentrations and [ 3 H]glucose specific activity. After the start of the insulin infusion, the plasma glucose concentration was allowed to decline to 5.
Plasma samples were collected every 15 min from 0—90 min and every 5—10 min from 90— min for the determination of plasma glucose and insulin concentrations and [ 3 H]glucose specific activity.
Plasma samples for the determination of GNG see below were taken before starting the [ 3 H]glucose infusion and at the end of the basal period. The glucose concentration was determined by the glucose oxidase method Beckman II Glucose Analyzer, Beckman, Fullerton, CA.
The plasma insulin concentration was measured by RIA Diagnostic Products, Los Angeles, CA. The serum HbA 1c concentration was measured by affinity chromatography biochemical methodology, Drower , Isolab, Akron, OH.
The plasma FFA concentration was measured spectrophotometrically Wako Chemicals GmbH, Neuss, Germany. The pattern of 2 H incorporation into plasma glucose after 2 H 2 O ingestion was determined according to the method developed by Landau and recently modified 20 , Briefly, the fraction of glucose produced via GNG from all precursors can be quantified from the ratio of 2 H enrichment of carbon 5 C5 to that of water.
The precursor of the hydrogen bound to C5 of glucose is the hydrogen bound to carbon 2 of glyceraldehydephosphate. That hydrogen equilibrates with the hydrogen of body water in the isomerization of glyceraldehydephosphate with dihydroxyacetone phosphate, an intermediate in the conversion of glycerol to glucose, and binds in the hydration of phosphoenolpyruvate formed in the conversion of pyruvate to glucose.
Because during glycogen breakdown there is no binding of hydrogen from body water to C5 of the glucose formed, enrichment at C5 in blood glucose vs. water reflects the fractional contribution of total GNG, i.
from both phosphoenolpyruvate precursors and glycerol. Plasma samples were first deproteinized using the Somogyi procedure. Samples were then reconstituted with μl distilled water and injected into a high performance liquid chromatograph Waters Corp.
Deuterium enrichment at C5 was obtained by converting glucose to xylose by the removal of carbon in position 6. Xylose was purified by HPLC; the C5 group was cleaved by oxidation with periodic acid, and formaldehyde was collected by distillation.
Formaldehyde was incubated with ammonia overnight. In the presence of ammonia, six molecules of formaldehyde react to form one molecule of hexamethylenetetramine. This step is used to increase the sensitivity of the method. Enrichment of hexamethylenetetramine obtained from C5 was determined by gas chromatography-mass spectrometry GCMS by monitoring peaks of mass and The precision and accuracy of C5 have been reported previously 8.
Water enrichment in the body water pool was monitored by reacting a sample of plasma or urine with calcium carbide CaC2 , thereby obtaining acetylene C2H2. The enrichment of acetylene was then determined by GCMS by monitoring peaks with masses of 26 and 27 All samples were run through the GCMS processing in duplicate or triplicate.
Glucose fluxes and plasma clearance rates were expressed per kilogram of FFM. During the baseline period of the study 0— min , both the plasma glucose concentration and [ 3 H]glucose specific activity were stable during the last 30 min of tracer infusion in all subjects.
Therefore, total EGO was calculated as the ratio of the [ 3 H]glucose infusion rate to the plasma [ 3 H]glucose specific activity mean of five determinations. At low rates of insulin-stimulated glucose disposal similar to those observed in the diabetic subjects in the present study , we have shown that the tracer-derived rates of Ra and Rd closely approximate the independently measured rates of whole body glucose disposal and glucose appearance Therefore, [ 3 H]glucose was not added to the exogenously infused glucose during the insulin clamp EGO during the insulin clamp was obtained as the difference between Ra and the exogenous glucose infusion rate.
Fasting plasma glucose clearance was calculated as the ratio between EGO and FPG, whereas insulin-mediated plasma glucose clearance was obtained as the ratio of Rd to plasma glucose concentration during the clamp.
Data are given as the mean ± se. A comparison of group values was performed using ANOVA with Bonferroni-Dunn post hoc testing. To factor out confounding variables, multivariate analysis was performed with the use of mixed models, including both continuous [age and body mass index BMI ] and nominal ethnicity, sex, and sulfonylurea treatment variables as independent variables; contrasts were used to estimate differences among levels of a nominal variable i.
tertiles of fasting glycemia or VF area. The strength of confounder-adjusted associations between the two variables of interest was expressed as the partial correlation coefficient. To examine the association between VF and metabolic control, the study cohort was divided into tertiles of fasting hyperglycemia.
Thus, group 1 included mildly hyperglycemic subjects, group 2 consisted of patients with moderate hyperglycemia, and group 3 included severely hyperglycemic patients Table 1. Except for a slight imbalance in sex distribution, the three groups were well matched for age, obesity BMI and percent fat mass , body fat distribution as determined by waist circumference and waist to hip ratio , and previous sulfonylurea treatment.
The serum lipid profile and arterial blood pressure levels were not significantly different among groups. Clinical characteristics in type 2 diabetic patients stratified by tertiles of fasting hyperglycemia.
MA, Mexican-American; HDL, high-density lipoprotein; LDL, low-density lipoprotein. As measured by MRI, abdominal SF area was similar across groups, whereas abdominal VF area was significantly greater in subjects with moderate to severe fasting hyperglycemia than in the mildly hyperglycemic subjects.
group 2. In the whole cohort, VF increased with age in both males and females and with indexes of fatness, whereas SF was positively related only to fatness Table 2. In the latter model, Mexican-American ethnicity and diabetes duration also were significant positive correlates of HbA 1c.
With regard to glucose fluxes, EGO was progressively higher, and plasma glucose clearance was progressively lower across groups both during the fasting state and under insulinized conditions Table 3.
In contrast, the relation of EGO to VF was weak and not statistically significant Fig. Plasma insulin and FFA concentrations were similar in the three groups both at baseline and during the clamp.
Inverse relationship between insulin-stimulated glucose clearance top panel or EGO bottom panel and VF area in 63 patients with type 2 diabetes. The fitting line and r value are those of a power function. Metabolic data in type 2 diabetic patients stratified by tertiles of fasting hyperglycemia.
P value for the difference among groups after adjustment by sex, age, ethnicity, BMI, and sulfonylurea treatment. In the subgroup of subjects 48 of 63 in whom GNG was measured, fasting EGO varied through FPG tertiles with a similar trend as in the whole cohort.
This increment was entirely due to increased GNG Table 4. To examine whether VF contributed to enhance GNG, the percent GNG was regressed against VF, first singly and then after adjustment for confounders. The inverse relationship between GLY and VF explains the lack of relationship between total EGO and VF.
Components of fasting glucose production in type 2 diabetic patients stratified by tertile of fasting hyperglycemia. Association of VF accumulation with gluconeogenic and glycogenolytic flux in 48 patients with type 2 diabetes.
The lines connect the observed values plotted as the mean ± sem at each tertile of VF area. In the whole cohort, fasting plasma FFA levels were independently i.
There was, however, no relationship between circulating FFA levels and either VF or SF. In this cohort of type 2 diabetic patients with an average disease duration of 5 yr and a wide range of fasting plasma glucose and HbA 1c levels, VF accumulation was clearly associated with poor metabolic control Table 1.
Upon stratifying the subjects by fasting glycemia, the resulting clinical phenotype was quite homogeneous, not only in terms of age, serum lipids and blood pressure, but also in terms of overall body size and fat distribution. Only increased VF and, to a smaller extent, diabetes duration paralleled the increase in FPG.
In a multiple regression model, which accounted for sex, age, BMI, and SF, only VF, diabetes duration, and Mexican-American ethnicity, in that order, were significant positive correlates of FPG. Thus, if every other measured factor is the same, the selective accumulation of fat in the visceral area is a predictor of the severity of fasting hyperglycemia.
Most importantly, VF is associated not only with the degree of fasting hyperglycemia, but even more strongly and independently with HbA 1c. A healthful diet that is low in sugar laden, processed foods will also help a person lose weight and shift excess visceral fat. A healthful diet should include:.
Boiling, steaming, baking, and grilling foods will help to make meals healthier and lower in fat. A man with a waistline that measures 40 inches or more or a woman whose waistline measures 35 inches or more is likely to have stores of visceral fat. Men and women who fall into these categories might want to make an appointment with a doctor to have levels of visceral fat measured, discuss potential risks, and get advice on how to make health and lifestyle changes to reduce visceral fat levels.
Some doctors may carry out some blood and other tests, or refer individuals to a nutritionist or dietitian. Visceral fat is fat that we cannot see, so it is not always easy to know whether a person has an excess of it. Because the associated health risks can be severe, it is essential for those who suspect their visceral fat levels are high to seek advice from a health professional.
Usually, it is possible to avoid high levels of visceral fat by leading a healthy and active lifestyle. Those who do store dangerous amounts of visceral fat can reduce their levels by making positive changes to their lifestyle. Changes include eating a nutritious, low-fat diet, increasing the amount of exercise, and lowering stress levels.
It is not possible to spot-reduce back fat. If you lead a sedentary life you risk building up large amounts of visceral fat in your body. WHAT IS VISCERAL FAT?
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Medical News Today. Health Conditions Health Products Discover Tools Connect. What is the best way to get rid of visceral fat?
Metrics details. There are Reduce hypertension naturally many scenarios and pathways Visceral fat and nutrient metabolism can lead to Viscwral syndrome. Viseral paper reviews mechanisms by which the xnd of visceral adipose tissue VAT may Visceral fat and nutrient metabolism to the metabolic syndrome, Viscerwl explores Anti-carcinogenic foods paradigm of a critical VAT threshold CVATT. Exceeding the CVATT may result in a number of metabolic disturbances such as insulin resistance to glucose uptake by cells. Metabolic profiles of patients with visceral obesity may substantially improve after only modest weight loss. This could reflect a significant reduction in the amount of VAT relative to peripheral or subcutaneous fat depots, thereby maintaining VAT below the CVATT. The CVATT may be unique for each individual.
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