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What Is The Relationship Between Insulin Resistance And Hyperinsulinemia?

Insulin Resistance And Hyperinsulinemia: Is Hyperinsulinemia The Cart Or Thehorse?

Insulin Resistance And Hyperinsulinemia: Is Hyperinsulinemia The Cart Or Thehorse?

1. Diabetes Care. 2008 Feb;31 Suppl 2:S262-8. doi: 10.2337/dc08-s264. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or thehorse? Shanik MH(1), Xu Y, Skrha J, Dankner R, Zick Y, Roth J. (1)Division of Endocrinology, North Shore-Long Island Jewish Health System, Lake Success, New York, USA. Insulin resistance, recently recognized as a strong predictor of disease inadults, has become the leading element of the metabolic syndrome and renewed as afocus of research. The condition exists when insulin levels are higher thanexpected relative to the level of glucose. Thus, insulin resistance is bydefinition tethered to hyperinsulinemia. The rising prevalence of medicalconditions where insulin resistance is common has energized research into thecauses. Many causes and consequences have been identified, but the directcontributions of insulin itself in causing or sustaining insulin resistance have received little sustained attention. We examine situations where insulin itselfappears to be a proximate and important quantitative contributor to insulinresistance. 1) Mice transfected with extra copies of the insulin gene producebasal and stimulated insulin levels that are two to four times elevated. The miceare of normal weight but show insulin resistance, hyperglycemia, andhypertriglyceridemia. 2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release ofglucose-raising hormones, postulated as the culprits in early studies, havelargely been excluded by studies including continuous glucose monitoring. 3) Ratsand humans treated with escalating doses of insulin show both hyperinsulinemiaand insulin resistance. 4) The pulsatile administration of insulin (rather thancontinuous) results in reduced requi Continue reading >>

Hyperinsulinemia: Is It Diabetes?

Hyperinsulinemia: Is It Diabetes?

Is hyperinsulinemia a form of diabetes? Answers from M. Regina Castro, M.D. Hyperinsulinemia (hi-pur-in-suh-lih-NEE-me-uh) means the amount of insulin in your blood is higher than what's considered normal. Alone, it isn't diabetes. But hyperinsulinemia is often associated with type 2 diabetes. Insulin is a hormone that's normally produced by your pancreas, which helps regulate blood sugar. Hyperinsulinemia is a sign of an underlying problem. Hyperinsulinemia is most often caused by insulin resistance — a condition in which your body doesn't respond well to the effects of insulin. Your pancreas tries to compensate by making more insulin. Insulin resistance may eventually lead to the development of type 2 diabetes. This happens when your pancreas is no longer able to compensate by secreting the large amounts of insulin required to keep the blood sugar normal. Rarely, hyperinsulinemia is caused by: A rare tumor of the insulin-producing cells of the pancreas (insulinoma) Excessive numbers or growth of insulin-producing cells in the pancreas (nesidioblastosis) Hyperinsulinemia usually causes no signs or symptoms, except in people with insulinomas in whom hyperinsulemia can cause low blood sugar (hypoglycemia). Treatment of hyperinsulinemia is directed at the underlying problem. Continue reading >>

Relationship Of Insulin Resistance And Hyperinsulinemia To Blood Pressure During Pregnancy.

Relationship Of Insulin Resistance And Hyperinsulinemia To Blood Pressure During Pregnancy.

Relationship of insulin resistance and hyperinsulinemia to blood pressure during pregnancy. Department of Obstetrics and Gynecology, University of California Los Angeles School of Medicine, Harbor-UCLA Medical Center, Torrance, USA. J Matern Fetal Med 1997 Sep-Oct;6(5):308. The purpose of our study was to examine the relationship between insulin resistance and blood pressure during pregnancy and to determine to what extent insulin resistance is related to the subsequent development of pregnancy-induced hypertension. The study population consisted of 292 women who had serum insulin, glucose and insulin-glucose ratios determined at 26-28 weeks gestation in a fasting state and 1 hr after a 50-g oral glucose challenge. These were compared with blood pressures at 26-28 weeks gestation and in the late third trimester. A statistically significant correlation exists overall between (1) blood pressure at 26-28 weeks gestation and both fasting insulin and insulin-glucose ratios, as well as (2) systolic blood pressure at term and fasting insulin levels. However, when controlled for confounding variables including body mass index, race and age, no statistically significant relationship remained. The metabolic variables in patients with pregnancy-induced hypertension were not statistically different from the normotensive patients. In conclusion, this study demonstrates that insulin resistance and hyperinsulinemia are not major determinants of blood pressure during pregnancy. Continue reading >>

Insulin Resistance And Hyperinsulinemia

Insulin Resistance And Hyperinsulinemia

From the Department of Medicine, Stanford University School of Medicine, Stanford, California Corresponding author: Sun H. Kim, [email protected] Received 2008 Jan 7; Accepted 2008 Mar 26. Copyright 2008, American Diabetes Association Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See for details. This article has been cited by other articles in PMC. OBJECTIVERecently, it has been suggested that insulin resistance and hyperinsulinemia can exist in isolation and have differential impacts on cardiovascular disease (CVD). To evaluate this suggestion, we assessed the degree of discordance between insulin sensitivity and insulin response in a healthy, nondiabetic population. RESEARCH DESIGN AND METHODSInsulin sensitivity was quantified by determining the steady-state plasma glucose (SSPG) concentration during an insulin suppression test in 446 individuals. The integrated insulin response was calculated after a 75-g oral glucose challenge. We analyzed the correlation between insulin resistance and insulin response in addition to quantifying the proportion in quartiles of insulin response by quartiles of insulin sensitivity. Then we compared CVD risk factors between individuals within the same insulin sensitivity quartile but within different insulin response quartiles to evaluate the differential clinical impact of insulin resistance and hyperinsulinemia. RESULTSInsulin resistance and insulin response were highly correlated (r = 0.76, P < 0.001). A majority (95%) of the most insulin-resistant individuals (top SSPG quartile) were either in the highest insulin response quartile (71%) or second highest (24%). Similarly, 92% of the most insulin-sensitive individuals (lowest SSPG quart Continue reading >>

Hyperinsulinemia And Insulin Resistance: World's Biggest Killers?

Hyperinsulinemia And Insulin Resistance: World's Biggest Killers?

When we think about the world’s biggest killer, different things come to mind. Or possibly heart disease, cancer, or maybe even dementia? Well, those three chronic diseases are all good bets. But what if they are just the result of something else, and they all have a common cause? In that case, that common cause could be the world’s biggest killer – and it goes by the name of hyperinsulinemia. This article takes a look at the rapidly growing problem of hyperinsulinemia and insulin resistance, and how they affect our health . Insulin resistance is a term to describe when our body develops a resistance to the effects of the hormone insulin ( 1 ). As a result, we experience increasing blood sugar levels and higher levels of circulating insulin ( 2 , 3 ). Hyperinsulinemia refers to the situation where we have a constant elevation of insulin levels ( 4 ). The literal definition is simply an excess amount of insulin in the blood. Insulin resistance is the usual cause of hyperinsulinemia, and the resulting high insulin levels can be very damaging to our body ( 5 ). There is a strong connection between hyperinsulinemia and type 2 diabetes, but they are not the same thing. Type 2 diabetes occurs when the pancreas fails to produce enough insulin to maintain normal blood sugar levels ( 6 ). However, hyperinsulinemia refers to when the body is producing too much insulin to keep high blood sugar levels in check ( 7 ). Without adequate intervention, chronic hyperinsulinemia can lead to type 2 diabetes ( 8 ). But it must be remembered: hyperinsulinemia is associated with metabolic syndrome, and it’s harmful independently of diabetes. Key Point: Insulin resistance leads to hyperinsulinemia – excess amounts of circulating insulin in the body. As shown above, insulin resist Continue reading >>

What Is Hyperinsulinemia?

What Is Hyperinsulinemia?

Hyperinsulinemia describes an increased level of insulin in the blood. The condition is associated with glucose intolerance, obesity, hypertension and dyslipidemia, factors that are collectively referred to as the metabolic syndrome. Hyperinsulinemia is distinct from both diabetes or hyperglycemia, but it occurs as a result of early stage diabetes, which may progress to diabetes if it is not treated properly. Hyperinsulinemia leads to several conditions and these are described below. Hypoglycemia or low blood sugar Diabetes or uncontrolled blood sugar that fluctuates between a low and high level Increased risk of Polycystic Ovarian Syndrome (PCOS) Increased production of very low-density lipoproteins (VLDLs), referred to as hypertriglyceridemia. Increased risk of cardiovascular or heart disease Coronary artery disease – the high insulin level damages the endothelial cells that line the coronary arteries. Underactive thyroid gland Weight gain and lethargy Causes Insulin resistance is the primary cause of hyperinsulinemia. When a person has insulin resistance, the pancreas tries to compensate by producing more insulin. This may lead to type 2 diabetes, which occurs when the pancreas fails to produce enough insulin to regulate the blood sugar level adequately. In rare cases, a pancreatic tumor can cause hyperinsulinemia. A condition called nesidioblastosis, where there is an excess of the cells that produce insulin in the pancreas can also lead to hyperinsulinemia. Reviewed by Sally Robertson, BSc Further Reading Continue reading >>

Insulin Resistance And Hyperinsulinemia

Insulin Resistance And Hyperinsulinemia

Insulin resistance, recently recognized as a strong predictor of disease in adults, has become the leading element of the metabolic syndrome and renewed as a focus of research. The condition exists when insulin levels are higher than expected relative to the level of glucose. Thus, insulin resistance is by definition tethered to hyperinsulinemia. The rising prevalence of medical conditions where insulin resistance is common has energized research into the causes. Many causes and consequences have been identified, but the direct contributions of insulin itself in causing or sustaining insulin resistance have received little sustained attention. We examine situations where insulin itself appears to be a proximate and important quantitative contributor to insulin resistance. 1) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia. 2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release of glucose-raising hormones, postulated as the culprits in early studies, have largely been excluded by studies including continuous glucose monitoring. 3) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance. 4) The pulsatile administration of insulin (rather than continuous) results in reduced requirements for insulin. 5) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin. In summary, hyperinsulinemia is often both a result and a driver of insulin resistance. HORMONE REGULATES TISSUE SENSITIVITY— A ho Continue reading >>

Hyperinsulinemia And Insulin Resistance: Scope Of The Problem

Hyperinsulinemia And Insulin Resistance: Scope Of The Problem

Jason Fung Department of Medicine, Scarborough Hospital, CanadaAmy Berger Nutrition Institute, University of Bridgeport, United States Fung J, Berger A. Hyperinsulinemia and Insulin Resistance: Scope of the Problem. Journal of Insulin Resistance. 2016;1(1), a18. Hyperinsulinemia and Insulin Resistance: Scope of the Problem Copyright: 2016. The Author(s). Licensee: AOSIS.This is an Open Access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution,and reproduction in any medium, provided the original work is properly cited. At the beginning of the 20th century, infectious agents were the major causes of disease. The top three causes of death were pneumonia, tuberculosis and gastrointestinal infections. As a result of improved public sanitation and breakthrough developments in antimicrobial agents, these once formidable illnesses are now more rare and easily treated. In the 21st century, acute infectious diseases have been replaced by cardiovascular disease (CVD), cancer and diabetic complications as the most common causes of death. The explosion of knowledge in genetics led to the discovery of many diseases that resulted from single genetic mutations. However, many modern, non-infectious chronic illnesses the so-called diseases of civilisation do not fit the one gene, one disease paradigm. Genetics obviously plays a role in susceptibility to disease, but just as obviously, the meteoric rise of these modern diseases cannot be the result of genetics alone. Rather than unlucky genes, these conditions result from metabolic processes and cellular physiology derailed by poor diet, disrupted circadian rhythms, poor stress management, inadequate physical activity and other parameters by which modern lifesty Continue reading >>

Relation Between Insulin Resistance, Hyperinsulinemia, Postheparin Plasmalipoprotein Lipase Activity, And Postprandial Lipemia.

Relation Between Insulin Resistance, Hyperinsulinemia, Postheparin Plasmalipoprotein Lipase Activity, And Postprandial Lipemia.

1. Arterioscler Thromb Vasc Biol. 1995 Mar;15(3):320-4. Relation between insulin resistance, hyperinsulinemia, postheparin plasmalipoprotein lipase activity, and postprandial lipemia. Jeppesen J(1), Hollenbeck CB, Zhou MY, Coulston AM, Jones C, Chen YD, Reaven GM. (1)Department of Medicine, Stanford University School of Medicine, Palo Alto, Calif, USA. We examined the relation between insulin resistance, plasma glucose and insulinresponses to meals, lipoprotein lipase (LPL) activity, and postprandial lipemiain a population of 37 healthy nondiabetic individuals. Plasma glucose and insulinconcentrations were determined at frequent intervals from 8 AM through midnight(breakfast at 8 AM and lunch at noon); resistance to insulin-mediated glucosedisposal was determined by measuring the steady-state plasma glucose (SSPG)concentration at the end of a 180-minute infusion of glucose, insulin, andsomatostatin; LPL activity was quantified in postheparin plasma; and postprandialconcentrations of triglyceride (TG)-rich lipoproteins were assessed by measuring the TG and retinyl palmitate content in plasma and the Svedberg flotation index(Sf) > 400 and Sf 20 to 400 lipoprotein fractions. Significant simple correlationcoefficients were found between various estimates of postprandial lipemia andSSPG (r = .38 to .68), daylong insulin response (r = .37 to .58), daylong glucoseresponse (r = .10 to .39), and LPL activity (r = -.08 to -.58). However, whenmultiple regression analysis was performed, only SSPG remained independentlyassociated with both postprandial TG and retinyl palmitate concentrations. These data provide evidence that insulin resistance plays an important role inregulating the postprandial concentration of TG-rich lipoproteins, includingthose of intestinal origin. Continue reading >>

Link Between Insulin Resistance And Hyperinsulinemia: Inhibitors Of Phosphatidylinositol 3-kinase Augment Glucose-induced Insulin Secretion From Islets Of Lean, But Not Obese, Rats* | Endocrinology | Oxford Academic

Link Between Insulin Resistance And Hyperinsulinemia: Inhibitors Of Phosphatidylinositol 3-kinase Augment Glucose-induced Insulin Secretion From Islets Of Lean, But Not Obese, Rats* | Endocrinology | Oxford Academic

Wortmannin (5100 nm), a specific phosphatidyinositol 3-kinase inhibitor, augmented 8 mm glucose-induced insulin secretion from control Sprague Dawley rat islets in a dose-dependent manner. This effect persisted after its removal from the perifusion medium; however, this augmenting effect was reduced by the calcium channel inhibitor nitrendipine or by lowering the glucose level to 3 mm. Wortmannin amplified insulin release induced by the combination of 68 mm glucose plus 1 m carbachol; however, it had no effect on phorbol ester- or -ketoisocaproate-induced insulin secretion. The potentiating action of wortmannin on 8 mm glucose-induced release was duplicated by LY294002. Wortmannin had no effect on glucose usage rates or inositol phosphate accumulation in[ 3H]inositol-prelabeled islets. Of particular significance, although 50 nm wortmannin potentiated 8 mm glucose-induced secretion from islets of lean Zucker control rats, the fungal metabolite had little effect on 8 mm glucose-induced release from islets of insulin-resistant Zucker fatty rats. These findings support the concept that the same biochemical process, inhibition of phosphatidyinositol 3-kinase, that causes peripheral tissue insulin resistance enhances -cell sensitivity to glucose and produces a compensatory increase in insulin secretion from these cells. The efficacy of wortmannin depends on the in vivo status of the donors insulin signaling pathways. This elegant biochemical control mechanism in -cells ensures the maintenance of glucose homeostasis despite a reduction in insulin action on peripheral tissues. A SENSITIVE and dynamic balance between tissue sensitivity to insulin and the prevailing insulin concentration exists. In situations (prediabetes, obesity, and type 2 diabetes) characterized by the devel Continue reading >>

What Is The Evidence That Insulin Resistance In Type 2 Diabetes And In Metabolic Syndrome Is Not Caused By Hyperinsulinemia?

What Is The Evidence That Insulin Resistance In Type 2 Diabetes And In Metabolic Syndrome Is Not Caused By Hyperinsulinemia?

When I was a medical student at McGill in the late 1970s, we learned a straightforward explanation for the cause of Type 2 diabetes, the most common form of diabetes in adults, accounting for about 90 per cent of all diabetes cases. We were told the insulin resistance responsible for Type 2 diabetes was caused by high levels of insulin. Hyperinsulinemia–increased insulin levels in the blood–was said to “downregulate” insulin receptors, making cells with those receptors less responsive to the insulin message. From a physiology point of view, this makes perfect sense. It’s analogous to the development of tolerance that can happen with regular heroin use when a person no longer responds to the drug in the way they did initially. Sometime in the 1980s this explanation for the cause of insulin resistance was abandoned. Instead, the medical community adopted a new theory that insulin resistance comes first, and is behind high insulin levels in Type 2 diabetes. To overcome insulin resistance, the pancreas secretes larger-than-normal amounts of insulin, resulting in so-called “reactive hyperinsulinemia.” The cause of this insulin resistance is never clearly explained, although obesity, chronic inflammation, and genes are all said to contribute. When I ask prominent endocrinologists about how insulin resistance comes about in this new paradigm, they say, sometimes condescendingly: “It’s too complicated for a psychiatrist to understand.” That may be. But I’m also an engineer, and when I studied at the University of Waterloo the saying was “BBB”, short for “Bulls**t Baffles Brains.” I consider myself to be a critical thinker, so if the new explanation for what causes insulin resistance is incomprehensible to me, that’s probably because it’s nonsen Continue reading >>

The Inter-relationship Between Insulin Resistance And Hypertension

The Inter-relationship Between Insulin Resistance And Hypertension

, Volume 46, Supplement2 , pp 149159 | Cite as The Inter-Relationship between Insulin Resistance and Hypertension Insulin resistance and compensatory hyperinsulinaemia commonly occur in patients with untreated essential hypertension. The coexistence of insulin resistance and hypertension can be viewed as a cause-effect relationship (insulin resistance as a cause of hypertension or vice versa) or as a noncausal association. Insulin can increase blood pressure via several mechanisms: increased renal sodium reabsorption, activation of the sympathetic nervous system, alteration of transmembrane ion transport, and hypertrophy of resistance vessels. Conversely, hypertension can cause insulin resistance by altering the delivery of insulin and glucose to skeletal muscle cells, resulting in impaired glucose uptake. For example, hypertension can impair vasodilation of skeletal muscle as a result of vascular structural changes and rarefaction, and increased response to vasoconstrictor stimuli. Also, the prevalence of muscle type 2b fibres (fast twitch fibres) may contribute to the development of insulin resistance. The common pathogenetic mechanism for both insulin resistance and hypertension could be activation of the sympathetic nervous system. This results in vasoconstriction, and may contribute to the genesis of vascular structural changes and increase the number of fast twitch fibres. Finally, hypertension and insulin resistance can be viewed as a noncausal association, according to the following hypotheses: 1) they may represent 2 independent consequences of the same metabolic disorder (intracellular free calcium accumulation), or 2) insulin resistance is a genetic marker and/or a pathogenetic mechanism of multiple metabolic abnormalities frequently associated with hyperten Continue reading >>

Joe | Mobile

Joe | Mobile

Metabolic disorders (e.g. diabetes, obesity, and metabolic syndrome) have over the past three decades reached pandemic dimensions, affecting a large number of the world population ( Wild & Byrne 2006 , Lin & Sun 2010 ). Insulin resistance is a common aspect of a number of these metabolic pathologies, such as type 2 diabetes, and also a powerful parameter for predicting the incidence of cardiovascular diseases and cancer ( Shanik et al. 2008 ). Hyperinsulinemia is the hallmark of insulin resistance in mammals. For instance, a twofold increase in plasma insulin levels can induce insulin resistance in mice, resembling the pattern in insulin-resistant patients with pathological obesity or type 2 diabetes who show similar increases in insulin levels ( Shanik et al. 2008 ). As insulin resistance is common to a number of metabolic diseases of which the relationships are still poorly understood, it is difficult to study with respect to causal relationships and genetic factors that are involved. Current models used for the study of insulin resistance range from mutant rodents to obese monkeys ( Shafrir 2010 ). Although these models reproduce the human situation with regard to obesity and insulin resistance, there still appear to be many conflicting results compared with the human situation, mainly due to the heterogeneity of the metabolic states where insulin resistance is observed ( Harano et al. 2002 , Kahn 2003 , Steinberger & Daniels 2003 ). The zebrafish (Danio rerio) is emerging as a model for deciphering the mechanisms underlying pathologies caused by an altered metabolism ( Seth et al. 2013 ). Principles of energy expenditure and metabolism are evolutionarily conserved in metazoans ( Schlegel & Stainier 2007 ). In addition, zebrafish larvae at 4 days post fertilization Continue reading >>

Insulin Resistance/compensatory Hyperinsulinemia, Essential Hypertension, And Cardiovascular Disease

Insulin Resistance/compensatory Hyperinsulinemia, Essential Hypertension, And Cardiovascular Disease

Insulin Resistance/Compensatory Hyperinsulinemia, Essential Hypertension, and Cardiovascular Disease Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305 Address all correspondence and requests for reprints to: Gerald Reaven, M.D., Falk Cardiovascular Research Center, Stanford Medical Center, 300 Pasteur Drive, Stanford, California 94305. Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 6, 1 June 2003, Pages 23992403, Gerald M. Reaven; Insulin Resistance/Compensatory Hyperinsulinemia, Essential Hypertension, and Cardiovascular Disease, The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 6, 1 June 2003, Pages 23992403, In 1966, Welborn et al. ( 1 ) studied 19 nondiabetic patients with essential hypertension and demonstrated that these individuals had significantly higher plasma insulin concentrations compared with a normotensive control group. Although these observations suggested that the prevalence of resistance to insulin-mediated glucose disposal would be increased in patients with essential hypertension, it wasnt until approximately 20 yr later that several research groups demonstrated that this was the case ( 2 7 ). Although the relationship between insulin resistance, hyperinsulinemia, and essential hypertension has been extensively studied in the past 15 yr, questions continue to be raised as to the nature of the link between these variables. Indeed, there is not even consensus as to whether or not there is a physiological relationship between insulin resistance/compensatory hyperinsulinemia and blood pressure regulation. Another issue, and perhaps of greater clinical relevance, is whether the insulin resistance/compensatory hyperinsu Continue reading >>

Hyperinsulinemia

Hyperinsulinemia

Tweet Hyperinsulinemia is often associated with type 2 diabetes, but it isn’t diabetes as such. Hyperinsulinemia means that the amount of insulin in the blood is higher than considered normal amongst non-diabetics. When a person has hyperinsulinemia they have a problem controlling blood sugar, meaning that the pancreas has to secrete larger amounts of insulin to keep blood sugar at a normal level. How is hyperinsulinemia caused? Insulin resistance is the primary cause of hyperinsulinemia, with the pancreas compensating by producing more insulin. Insulin resistance of this type can lead to the development of type 2 diabetes, which occurs when the pancreas cannot secrete the insulin required to maintain normal blood glucose levels. In more rare cases, hyperinsulinemia may be caused by a tumour of the insulin-producing cells of the pancreas (insulinoma). It may also be caused by excessive numbers of insulin-producing cells in the pancreas (nesidioblastosis). What are the risks of having hyperinsulinemia? There are a number of risks involved in having hyperinsulinemia which include: Higher triglyceride levels High uric acid Hardening of the arteries (artherosclerosis) Weight gain Hypertension Type 2 diabetes The sooner hyperinsulinemia is diagnosed, which may be in the form of pre-diabetes or type 2 diabetes, the sooner the risks or extent of the above can be reduced. What are the symptoms of hyperinsulinemia? Although hyperinsulinemia often has little clear indicator, hyperinsulinemia symptoms may include: Weight gain Cravings for sugar Intense hunger Feeling frequently hungry Difficulty concentrating Feeling anxious or panicky Lacking focus or motivation Fatigue How is hyperinsulinemia treated? Medical treatment, in the form of diabetes medication, may help to relieve t Continue reading >>

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