Glucose fesponse. CIs nutrition for triathletes change differences nutrition for triathletes treatments in Gllucose and secondary outcomes 6-month changes were assessed by using two-sample Welsh unequal variance t test, where the outcome distribution was assumed to be normal. Physiology, Adenosine Triphosphate. Butter was replaced with coconut oil and sugar was partially replaced with a low GI sweetener.

Glucose response -

The peripheral plasma concentrations of glucose, insulin, glucagon, alpha amino nitrogen, urea nitrogen, free fatty acids, and triglycerides were measured. Following ingestion of the meals containing protein, the plasma insulin concentration was increased further and remained elevated longer compared with the meal containing glucose alone.

The glucose response was diminished following ingestion of the meals containing protein with the exception of the egg white meals. The peripheral glucagon concentration was decreased following ingestion of glucose alone and increased following all the meals containing protein.

The alpha amino nitrogen concentration varied considerably. Yep, weight gain. You do not have to be overweight to have insulin resistance. If you have insulin resistance, you want to become the opposite—more insulin sensitive cells are more effective at absorbing blood sugar so less insulin is needed.

These lifestyle changes really work. Talk with your health care provider about how to get started. Skip directly to site content Skip directly to search. Español Other Languages. Insulin Resistance and Diabetes. Spanish Print. Minus Related Pages.

Insulin acts like a key to let blood sugar into cells for use as energy. Insulin, Blood Sugar, and Type 2 Diabetes Insulin is a key player in developing type 2 diabetes.

Here are the high points: The food you eat is broken down into blood sugar. Blood sugar enters your bloodstream, which signals the pancreas to release insulin. Amylin analogues have been created and are available through various pharmaceutical companies as a solution for disorders of this hormone.

Incretins go to work even before blood glucose levels rise following a meal. They also slow the rate of absorption of nutrients into the bloodstream by reducing gastric emptying, and they may also help decrease food intake by increasing satiety.

People with type 2 diabetes have lower than normal levels of incretins, which may partly explain why many people with diabetes state they constantly feel hungry.

After research showed that BG levels are influenced by intestinal hormones in addition to insulin and glucagon, incretin mimetics became a new class of medications to help balance BG levels in people who have diabetes. Two types of incretin hormones are GLP-1 glucagon-like peptide and GIP gastric inhibitory polypeptide.

Each peptide is broken down by naturally occurring enzymes called DDP-4, dipeptidyl peptidase Exenatide Byetta , an injectable anti-diabetes drug, is categorized as a glucagon-like peptide GLP-1 and directly mimics the glucose-lowering effects of natural incretins upon oral ingestion of carbohydrates.

The administration of exenatide helps to reduce BG levels by mimicking the incretins. Both long- and short-acting forms of GLP-1 agents are currently being used. A new class of medications, called DPP4 inhibitors, block this enzyme from breaking down incretins, thereby prolonging the positive incretin effects of glucose suppression.

An additional class of medications called dipeptidyl peptidase-4 DPP-4 inhibitors—note hyphen , are available in the form of several orally administered products. These agents will be discussed more fully later. People with diabetes have frequent and persistent hyperglycemia, which is the hallmark sign of diabetes.

For people with type 1 diabetes, who make no insulin, glucose remains in the blood plasma without the needed BG-lowering effect of insulin. Another contributor to this chronic hyperglycemia is the liver.

When a person with diabetes is fasting, the liver secretes too much glucose, and it continues to secrete glucose even after the blood level reaches a normal range Basu et al. Another contributor to chronic hyperglycemia in diabetes is skeletal muscle.

After a meal, the muscles in a person with diabetes take up too little glucose, leaving blood glucose levels elevated for extended periods Basu et al.

The metabolic malfunctioning of the liver and skeletal muscles in type 2 diabetes results from a combination of insulin resistance, beta cell dysfunction, excess glucagon, and decreased incretins.

These problems develop progressively. Early in the disease the existing insulin resistance can be counteracted by excess insulin secretion from the beta cells of the pancreas, which try to address the hyperglycemia. The hyperglycemia caused by insulin resistance is met by hyperinsulinemia.

Eventually, however, the beta cells begin to fail. Hyperglycemia can no longer be matched by excess insulin secretion, and the person develops clinical diabetes Maitra, How would you explain to your patient what lifestyle behaviors create insulin resistance?

In type 2 diabetes, many patients have body cells with a decreased response to insulin known as insulin resistance. This means that, for the same amount of circulating insulin, the skeletal muscles, liver, and adipose tissue take up and metabolize less glucose than normal.

Insulin resistance can develop in a person over many years before the appearance of type 2 diabetes. People inherit a propensity for developing insulin resistance, and other health problems can worsen the condition. For example, when skeletal muscle cells are bathed in excess free fatty acids, the cells preferentially use the fat for metabolism while taking up and using less glucose than normal, even when there is plenty of insulin available.

In this way, high levels of blood lipids decrease the effectiveness of insulin; thus, high cholesterol and body fat, overweight and obesity increase insulin resistance.

Physical inactivity has a similar effect. Sedentary overweight and obese people accumulate triglycerides in their muscle cells. This causes the cells to use fat rather than glucose to produce muscular energy. Physical inactivity and obesity increase insulin resistance Monnier et al.

For people with type 1 diabetes, no insulin is produced due to beta cells destruction. Triggers of that autoimmune response have been linked to milk, vaccines, environmental triggers, viruses, and bacteria.

For people with type 2 diabetes, a progressive decrease in the concentration of insulin in the blood develops. Not only do the beta cells release less insulin as type 2 diabetes progresses, they also release it slowly and in a different pattern than that of healthy people Monnier et al.

Without sufficient insulin, the glucose-absorbing tissues—mainly skeletal muscle, liver, and adipose tissue—do not efficiently clear excess glucose from the bloodstream, and the person suffers the damaging effects of toxic chronic hyperglycemia. At first, the beta cells manage to manufacture and release sufficient insulin to compensate for the higher demands caused by insulin resistance.

Eventually, however, the defective beta cells decrease their insulin production and can no longer meet the increased demand. At this point, the person has persistent hyperglycemia.

A downward spiral follows. The hyperglycemia and hyperinsulinemia caused by the over-stressed beta cells create their own failure.

In type 2 diabetes, the continual loss of functioning beta cells shows up as a progressive hyperglycemia. How would you explain insulin resistance differently to someone with type 1 diabetes and someone with type 2 diabetes?

Together, insulin resistance and decreased insulin secretion lead to hyperglycemia, which causes most of the health problems in diabetes. The acute health problems—diabetic ketoacidosis and hyperosmolar hyperglycemic state—are metabolic disorders that are directly caused by an overload of glucose.

In comparison, the chronic health problems—eye, heart, kidney, nerve, and wound problems—are tissue injury, a slow and progressive cellular damage caused by feeding tissues too much glucose ADA, Hyperglycemic damage to tissues is the result of glucose toxicity.

There are at least three distinct routes by which excess glucose injures tissues:. If you are attending a virtual event or viewing video content, you must meet the minimum participation requirement to proceed. If you think this message was received in error, please contact an administrator. You are here Home » Diabetes Type 2: Nothing Sweet About It.

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During stressful situations, epinephrine Plyometric training for athletesGlucose response, growth hormone and nutrition for triathletes play a role Gluxose blood sugar levels. Stressful situations include infections, serious illness or Gluccose emotion stress. When stressed, the body prepares itself by ensuring that respponse sugar or energy is readily available. Insulin levels fall, glucagon and epinephrine adrenaline levels rise and more glucose is released from the liver. At the same time, growth hormone and cortisol levels rise, which causes body tissues muscle and fat to be less sensitive to insulin. As a result, more glucose is available in the blood stream. When you have type 2 diabetes, low blood sugars from too much medication or insulin are a common cause of stress.

Glucose response -

It's important to eat and drink normally in the days leading up to the glucose tolerance test. Let your doctor know if you're ill or taking any medications, as these factors can affect the results of your test.

For eight hours before the test, you won't be able to eat or drink anything. You might want to fast overnight and schedule the test for early the following morning. The glucose tolerance test is done in several steps.

When you arrive at your doctor's office or lab, a member of your health care team will take a sample of blood from a vein in your arm. This blood sample will be used to measure your fasting blood glucose level. The American College of Obstetricians and Gynecologists recommends performing a one-hour blood glucose challenge test to screen for gestational diabetes in low-risk pregnant women between 24 and 28 weeks of pregnancy.

Your doctor may recommend earlier screening if you're at increased risk of developing gestational diabetes. Risk factors may include:. If your doctor determines you're at risk or you have a suspicious value on the one-hour test, you may be advised to take a three-hour glucose tolerance test.

After drinking the glucose solution, you'll likely need to remain in the doctor's office or lab while you're waiting for your blood glucose level to be tested.

If the results of your glucose tolerance test indicate type 2 diabetes, your doctor may repeat the test on another day or use another blood test to confirm the diagnosis.

Various factors can affect the accuracy of the glucose tolerance test, including illness, activity level and certain medications. If you're being tested for gestational diabetes, your doctor will consider the results of each blood glucose test.

If one of the results is higher than normal, you'll likely need to test again in four weeks. If two or more of the results are higher than normal, you'll be diagnosed with gestational diabetes. If you're diagnosed with gestational diabetes, you can prevent complications by carefully managing your blood glucose level throughout the rest of your pregnancy.

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This content does not have an English version. This content does not have an Arabic version. Overview The glucose tolerance test, also known as the oral glucose tolerance test, measures your body's response to sugar glucose. More Information Diabetes Dumping syndrome Gestational diabetes Polycystic ovary syndrome PCOS Prediabetes Type 2 diabetes Type 2 diabetes in children Show more related information.

Request an appointment. Thank you for subscribing! Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry. By Mayo Clinic Staff. Show references Glucose tests. Lab Tests Online. The endocrine functionality of the pancreas regulates glucose homeostasis.

Liver: Glycogenesis and gluconeogenesis are the storing and releasing of glucose, respectively. These processes occur using insulin, glucagon, and hepatocyte derived factors. Gut: Hormones in the gut are released in response to the ingestion of nutrients.

These hormones are involved in appetite, glucose production, gastric emptying, and glucose removal. Adipocytes: Adipose tissue secretes adipokines, which regulate insulin release through their involvement in glucose metabolism, control of food intake, and insulin gene expression.

Function Glucose metabolism involves multiple processes, including glycolysis, gluconeogenesis, glycogenolysis, and glycogenesis. Mechanism Glycolysis is the most crucial process in releasing energy from glucose, the end product of which is two molecules of pyruvic acid.

Related Testing HbA1c. Since the HbA1C value summarizes long-term glycemic control, it is frequently used to evaluate patients with long-standing hyperglycemia, as seen in patients with diabetes, and to forecast the risk of diabetic complications. Fasting Plasma Glucose.

Plasma blood glucose level is measured after a period of fasting, typically at least 8 hours. Random Plasma Glucose. A random plasma glucose measurement is sampled sometime after dietary intake was last ingested.

Oral Glucose Tolerance Test. All pregnant women should receive gestational diabetes mellitus GDM screening through an orally consumed glucose challenge and subsequent plasma blood glucose measurement.

Measured via urine or serum samples, a C-peptide value aids in the evaluation and management of diabetes. The presence of autoantibodies, including islet autoantibody, insulin autoantibody, insulinoma-associated antigen-2 autoantibodies, and anti-glutamic acid decarboxylase GAD autoantibodies, among others, are suggestive of auto-immune response as is seen in type 1 diabetes.

Pathophysiology Although not completely understood, Type 1 and Type 2 diabetes differ in their pathophysiology. Clinical Significance Poor glucose metabolism leads to diabetes mellitus. Diabetes is classified into two types- Type 1 DM- due to deficient insulin secretion. Circulating insulin is virtually absent, leading to a catabolic state with exogenous insulin required for treatment.

This condition occurs predominantly in adults but is now increasingly present in children and adolescents.

Review Questions Access free multiple choice questions on this topic. Comment on this article. Figure Diagram of the relationship between the processes of carbohydrate metabolism, including glycolysis, gluconeogenesis, glycogenesis, glycogenolysis, fructose metabolism, and galactose metabolism Contributed by Wikimedia User: Eschopp, CC BY-SA 4.

References 1. Jaiswal N, Gavin MG, Quinn WJ, Luongo TS, Gelfer RG, Baur JA, Titchenell PM. The role of skeletal muscle Akt in the regulation of muscle mass and glucose homeostasis. Mol Metab. Chen Y, Zhao X, Wu H. Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus: The Role of Protein O -GlcNAc Modification.

Arterioscler Thromb Vasc Biol. Taneera J, Dhaiban S, Mohammed AK, Mukhopadhyay D, Aljaibeji H, Sulaiman N, Fadista J, Salehi A. GNAS gene is an important regulator of insulin secretory capacity in pancreatic β-cells. Hay WW. Placental-fetal glucose exchange and fetal glucose metabolism.

Trans Am Clin Climatol Assoc. Schaefer-Graf U, Napoli A, Nolan CJ. Diabetes in pregnancy: a new decade of challenges ahead. Röder PV, Wu B, Liu Y, Han W. Pancreatic regulation of glucose homeostasis.

Exp Mol Med. Han HS, Kang G, Kim JS, Choi BH, Koo SH. Regulation of glucose metabolism from a liver-centric perspective.

Poggiogalle E, Jamshed H, Peterson CM. Circadian regulation of glucose, lipid, and energy metabolism in humans. Tozzi M, Hansen JB, Novak I. Pannexin-1 mediated ATP release in adipocytes is sensitive to glucose and insulin and modulates lipolysis and macrophage migration.

Acta Physiol Oxf. Schnell O, Crocker JB, Weng J. Impact of HbA1c Testing at Point of Care on Diabetes Management. J Diabetes Sci Technol. Eun YM, Kang SG, Song SW. Fasting plasma glucose levels and coronary artery calcification in subjects with impaired fasting glucose.

Ann Saudi Med. Barasch A, Gilbert GH, Spurlock N, Funkhouser E, Persson LL, Safford MM. Random plasma glucose values measured in community dental practices: findings from the dental practice-based research network. Tex Dent J. Garrison A. Screening, diagnosis, and management of gestational diabetes mellitus.

Am Fam Physician. Leighton E, Sainsbury CA, Jones GC. A Practical Review of C-Peptide Testing in Diabetes. Diabetes Ther. Regnell SE, Lernmark Å. Early prediction of autoimmune type 1 diabetes.

Pippitt K, Li M, Gurgle HE. Diabetes Mellitus: Screening and Diagnosis. Skyler JS, Bakris GL, Bonifacio E, Darsow T, Eckel RH, Groop L, Groop PH, Handelsman Y, Insel RA, Mathieu C, McElvaine AT, Palmer JP, Pugliese A, Schatz DA, Sosenko JM, Wilding JP, Ratner RE.

Differentiation of Diabetes by Pathophysiology, Natural History, and Prognosis. Zhang N, Jiang H, Bai Y, Lu X, Feng M, Guo Y, Zhang S, Luo Q, Wu H, Wang L. Commonly consumed foods by PPT participants included tahini, eggs, nuts, high-fat cheese, vegetables, chicken, beef, and fish Supplementary Fig.

As expected, the PPT diet resulted in a relatively low average carbohydrate content since dietary carbohydrates are considered a major factor of PPGR prediction. Furthermore, for each person, meals with a similar amount of carbohydrates but different food components yielded different PPGR predictions and thus promoted different recommendations, such that two meals with the same amount of carbohydrates could generate different scores and result in distinct actual PPGR in the same participant Supplementary Fig.

Consistent with this notion, changes in dietary carbohydrate intake during the intervention only modestly correlated with changes in primary outcomes Supplementary Fig. As designed, there was no significant difference in physical activity level between the groups mean ± SD 1. Among the participants included in the primary analysis, there was a significant decrease in both time above and HbA 1c at the end of the intervention.

In a sensitivity analysis of six imputation methods, the results remained statistically significant for time above and HbA 1c Supplementary Fig. We also performed post hoc subgroup analyses for the difference between treatments in subgroups by age, BMI, sex, and compliance.

CIs for between-group change difference in primary and secondary outcomes. A : Primary outcomes. B : Secondary outcomes. BP dia, diastolic blood pressure; BP sys, systolic blood pressure; US, ultrasound.

The changes in primary outcomes over time are shown in Fig. Changes in primary and selected secondary outcomes during the intervention phase. A : Changes in primary outcomes over time in the MED diet and PPT diet. Analysis was done based on intention-to-treat principle.

To statistically evaluate the changes in outcomes over time, the repeated-measures ANOVA test was used, and the difference between groups at each time point was assessed by t test.

B : Changes in three selected secondary outcomes over time in the MED diet and PPT diet. To evaluate the differences between groups at each time point, a t test was used for weight and triglycerides, and a Mann-Whitney nonparametric test was used for total cholesterol-to-HDL cholesterol ratio.

Chol, cholesterol. Changes in secondary outcomes at the end of the intervention 6 months are shown in Figs. For other glycemic measurements, including FPG, insulin, and HOMA-IR, no significant differences were noted between the groups Fig.

Additional secondary outcomes, including total cholesterol, blood pressure, liver enzymes ALT, AST , hepatic ultrasound, and anthropometric measurements weight, BMI, fat percentage demonstrated significant reductions in each group compared with its own baseline, but these did not reach significant differences between groups Fig.

At the end of the intervention, the average weight loss observed was 2. The changes in all secondary outcomes over time are shown in Fig.

For other secondary outcomes, there was no significant interaction between diet group and time. In other secondary outcomes, there was no significant difference between the groups at 12 months Supplementary Fig. During the monthly individual dietary follow-up meetings, dietitians asked participants about tolerance and side effects related to the diet, including bloating, fullness, indigestion, or any other diet-related symptoms.

Only temporary complaints were reported, and these were solved satisfactorily by standard dietary advice on eating patterns. In some cases, the symptoms were resolved by the use of barrier products e.

In these cases, we used the CGM data collected up to that time point and continued to collect other trial measures as usual, including dietary records, blood tests, and all other measurements.

Other glycemic and metabolic measures also improved significantly more with the PPT diet, including 5-h PPGR excursions, mean CGM glucose, blood fructosamine, FLI, blood triglycerides, HDL cholesterol, and total cholesterol-to-HDL cholesterol ratio, demonstrating another potential benefit of the PPT approach in reducing cardiometabolic risks in prediabetes 1.

These findings suggest that a dietary strategy focused on PPGR reductions is safe and effective for helping to improve glycemic control in prediabetes. At month follow-up, the significant difference in glycemic control between the groups was maintained, suggesting that personalized PPGR-targeting diets may have long-term efficacy in improving blood glucose levels.

Our findings support the general importance and beneficial effects of lifestyle modifications for diabetes prevention in prediabetes, as previously demonstrated in the DPP 4. While glycemia improved as measured by both time above and HbA 1c , the results of a single OGTT at 6 months were not significantly different between the groups.

This may be due to significant variability in the postprandial response to a single standard carbohydrate challenge compared with multiple other real-world meals over time.

Alternatively, other biological mechanisms or study methodological aspects may explain this result, which requires further investigation in future studies. Advantages of this trial design include the use of CGM throughout the entire intervention period, which allowed us to directly measure the effects of every meal on glucose levels while evaluating the importance of long-term reductions in PPGRs to metabolic health.

As such, and in contrast to blood tests, which provide a single point-of-care measure that may be sensitive to test errors, long-term CGM data may provide a more accurate reflection of the glycemic state. Indeed, the use of CGM in the research setting and clinical practice for diabetes management is becoming more common Additionally, full dietary records logged by the study participants using a designated smartphone app allowed us to closely monitor compliance and diet adherence by participants in both arms while de facto assessing the distinction between the two dietary treatments.

The fact that the two groups had a similar number of calories reported on average during the intervention, along with similar modest weight loss rates observed in both groups, suggests that the dietary records were indeed reliable.

We find that this approach enables a major advantage. Typical dietary intake assessment in clinical trials is done by using food frequency questionnaires or occasional h recalls and food diaries, which inaccurately assess actual dietary consumption throughout the intervention period, thereby limiting the ability to draw precise conclusions about health outcomes of different dietary approaches.

Our study also has several limitations. We compared only two dietary approaches: a MED diet and our algorithm-based PPT diet. Since carbohydrate content of the meal constitutes an important component in the PPGR prediction algorithm, the PPT diet resulted in lower carbohydrate content on average compared with the MED diet.

Thus, it is possible that the beneficial effects observed in the PPT diet are mainly driven by the lower carbohydrate content. However, we speculate that this is not the case because the change in dietary carbohydrate intake during the intervention was not highly correlated with primary clinical outcomes e.

Furthermore, other studies demonstrated that low-carbohydrate diets are not superior to high-carbohydrate diets in terms of long-term glycemic control or weight management 14 , In a systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes, Snorgaard et al.

Gardner et al. Finally, beyond the overall macronutrient composition of the diet, the PPT diet enabled an individualized set of recommendations at the level of meals, regardless of their carbohydrate content, such that identical meals yielded different recommendation levels for different people Supplementary Fig.

Nevertheless, differences between our algorithmbased PPT diet and other low-carbohydrate diets should be further explored. These limitations notwithstanding, in this randomized clinical trial in prediabetes, a personalized PPT diet improved glycemic control significantly more than a MED diet.

These findings may have implications for prediabetes dietary advice in clinical practice and potentially for other metabolic disorders, including type 2 diabetes, metabolic syndrome, and nonalcoholic fatty liver disease, pending rigorous clinical testing to generate evidence of benefit in these clinical conditions.

Clinical trial reg. NCT, clinicaltrials. The authors thank the Segal group members for fruitful discussions; Dr. David Zeevi Center for Studies in Physics and Biology, The Rockefeller University, New York, NY and Dr.

Tal Korem Program for Mathematical Genomics, Department of Systems Biology, Columbia University Irving Medical Center, New York, NY , former laboratory members, for fruitful discussions and critical insights to the trial design and manuscript; Dr.

Relly Abel from Clalit Health Services and Billy Cohen from Maccabi Healthcare Services for help with recruitment of participants; Ofra Lavi from AMC Medical Center Laboratory for operating all processes of blood tests at the central laboratory of the trial; Rachel Segall for coordinating collaboration with AMC Medical Center Laboratory; and Anat Schneider, Maya Ahimas, and Shikma Shor The Robert H.

Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem for help with phone calls to candidates during registration and enrollment procedures. Duality of Interest. The funding for the study was provided jointly by the companies Janssen Pharmaceuticals, Inc.

Janssen is one of the investors of DayTwo. and E. are regular paid consultants for DayTwo. No other potential conflicts of interest relevant to this article were reported.

No pharmaceutical manufacturers or other companies from the industry, including the sponsors mentioned above, contributed to the planning, design, or conduct of the trial. The analyses presented here were performed by Weizmann scientists independent of the sponsors.

The scientists have the right to publish regardless of the outcome. Author Contributions. was the clinical trial lead, oversaw the conduct of the study, and wrote the manuscript.

and A. designed and directed the project and data collection and analyses, interpreted the results, and contributed equally to the study. conceived the study and designed the intervention.

provided dietary recommendations and personal dietetic support throughout the intervention to all study participants. directed all computational aspects of the study, with support from D. was the medical lead of the study with support from N. and N.

coordinated participant recruitment and management throughout the intervention and follow-up. conceived and directed the project and analyses, designed the analyses, interpreted the results, and wrote the manuscript.

All authors reviewed and approved the manuscript and vouch for the accuracy and completeness of the data. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

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Sustaining optimal gastrointestinal function glucose responsr Hydrostatic weighing and body shape analysis, biphasic and incessant increase responses. There are three Hydrostatic weighing and body shape analysis glucose curves: nutrition for triathletes, biphasic, Glucsoe incessant increase. Gluucose the underlying causes behind Glufose curves, their implications for health eesponse tips for improving your glucose responses. Grasping how our bodies react to food, particularly high-sugar meals, is essential for sustaining optimal health. Monophasic, biphasic and incessant increase glucose curves could indicate varying degrees of metabolic fitness, which can have significant consequences for glucose management. Research demonstrates that individuals with monophasic responses after consuming large amounts of carbohydrates may have a lower metabolic health profile. This may include:. gov means it's GGlucose. Federal government websites often end Glucose response. gov or. Before sharing sensitive information, make sure you're on a federal government site. The site is secure.