MODY is an autosomal, dominantly inherited form of diabetes that is characterized by an early age of onset (at least one affected family member with an onset before 25 years of age) and pancreatic beta-cell dysfunction. Linkage between microsatellite markers and disease was described in French and UK pedigrees and the first mutation was reported in 1992. MODY has been associated with defects in several genes; glucokinase (GCK) was the first MODY gene to be identified. The prevalence of GCK-MODY is difficult to assess, as the mild hyperglycemia and the absence of symptoms means that patients are frequently not diagnosed.
In the Caucasian population, approximately 2% of the population will be diagnosed with gestational diabetes; of these, ~2-5% will have a GCK mutation.
Neonatal diabetes mellitus (NDM), caused by homozygous inactivating mutation, is a rare disorder with an estimated incidence of 1:400,000 live births. The glucokinase (GCK) gene encodes a 465 amino acid protein with a MW of 52 kDa, which is expressed in the pancreas, liver, and brain. The two isoforms of glucokinase differ by 13-15 amino acids at the N-terminal end of the molecule, which produces only a minimal difference in structure. In liver, glucokinase acts as the gateway for the "bulk processing" of available glucose, while in the neuroendocrine cells, it acts as a sensor, triggering cell responses that affect body-wide carbohydrate metabolism.
The presence of tissue-specific promoters allows differential regulation and transcription of different transcripts.
Heterozygous inactivating mutations are associated with mild hyperglycemia in children or gestational DM in women which are often subclinical and can be treated with diet alone. Homozygous inactivating mutation results in permanent neonatal diabetes and requires insulin treatment within the first month. Over 190 mutations of the GCK gene have been identified in many populations, with the majority in France and Italy.
Therapeutic intervention and prevention of progression of DPN have the greatest impact if instituted very early in the course of disease. The ADA recommends that all patients with diabetes should be screened at least annually for chronic sensorimotor DPN. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractType 2 diabetes mellitus (T2DM) has an intersecting underlying pathology with thyroid dysfunction. The literature is punctuated with evidence indicating a contribution of abnormalities of thyroid hormones to type 2 DM. The most probable mechanism leading to T2DM in thyroid dysfunction could be attributed to perturbed genetic expression of a constellation of genes along with physiological aberrations leading to impaired glucose utilization and disposal in muscles, overproduction of hepatic glucose output, and enhanced absorption of splanchnic glucose.
Huggins, “Effect of hyperthyroidism upon diabetes mellitus: striking improvement in diabetes mellitus from thyroidectomy,” Annals of Surgery, vol. Hyper- and hypothyroidism have been associated with insulin resistance which has been reported to be the major cause of impaired glucose metabolism in T2DM. The state-of-art evidence suggests a pivotal role of insulin resistance in underlining the relation between T2DM and thyroid dysfunction. A plethora of preclinical, molecular, and clinical studies have evidenced an undeniable role of thyroid malfunctioning as a comorbid disorder of T2DM. It has been investigated that specifically designed thyroid hormone analogues can be looked upon as the potential therapeutic strategies to alleviate diabetes, obesity, and atherosclerosis.
These molecules are in final stages of preclinical and clinical evaluation and may pave the way to unveil a distinct class of drugs to treat metabolic disorders.1. IntroductionThe role of hyperthyroidism in diabetes was investigated in 1927, by Coller and Huggins proving the association of hyperthyroidism and worsening of diabetes. Klein, “Potential therapeutic applications of thyroid hormone analogs,” Nature Clinical Practice Endocrinology and Metabolism, vol.
It was shown that surgical removal of parts of thyroid gland had an ameliorative effect on the restoration of glucose tolerance in hyperthyroid patients suffering from coexisting diabetes [1].There is a deep underlying relation between diabetes mellitus and thyroid dysfunction [2]. A plethora of studies have evidenced an array of complex intertwining biochemical, genetic, and hormonal malfunctions mirroring this pathophysiological association [2, 3]. 5′ adenosine monophosphate-activated protein kinase (AMPK) is a central target for modulation of insulin sensitivity and feedback of thyroid hormones associated with appetite and energy expenditure [3].
A meta-analysis reported a frequency of 11% in thyroid dysfunction in the patients of diabetes mellitus [4]. The relation between T2DM and thyroid dysfunction has been a less explored arena which may behold answers to various facts of metabolic syndrome including atherosclerosis, hypertension, and related cardiovascular disorders.T2DM owes its pathological origin to inappropriate secretion of insulin, due to defective islet cell function or beta cell mass.
Lanni, “Action of thyroid hormones at the cellular level: the mitochondrial target,” FEBS Letters, vol.
Continuous consumption of calories-rich meals, junk food and sedentary lifestyle have culminated into an epidemic of diabetes projected to afflict around 300 million people across the globe by 2020 [9]. Defective insulin secretion leads to various metabolic aberrations in T2DM, spanning from hyperglycemia due to defective insulin-stimulated glucose uptake and upregulated hepatic glucose production, along with dyslipidaemia, which includes impaired homeostasis of fatty acids, triglycerides, and lipoproteins [10].2. The prevalence of thyroid dysfunction is advancing with age all over the world, and frequency of prevalence was higher in women than men.
The prevalence of subclinical hypothyroidism is reported to be about 4 to 8.5 percent, and may be as high as 20 percent in women older than 60 years. Okosieme, “Thyroid dysfunction in patients with diabetes: clinical implications and screening strategies,” International Journal of Clinical Practice, vol.
Peripheral Effects of Thyroid Hormones on Insulin Secretion and SensitivityThyroid hormones directly control insulin secretion.
In hypothyroidism, there is a reduction in glucose-induced insulin secretion by beta cells, and the response of beta cells to glucose or catecholamine is increased in hyperthyroidism due to increased beta cell mass.
ThyrotoxicosisIncreased glucose output from liver is the pivotal reason for the induction of hyperinsulinaemia, induction of glucose intolerance, and development of peripheral insulin resistance [17]. Knip et al., “Other complications and associated conditions with diabetes in children and adolescents,” Pediatric Diabetes, vol.
Glucose tolerance in thyrotoxicosis is caused by elevated hepatic glucose output along with upregulated glycogenolysis [2].
This phenomenon is responsible for worsening of subclinical diabetes and exaggeration of hyperglycaemia in T2DM. Thyrotoxicosis may lead to ketoacidosis also due to elevated lipolytic actions and increased hepatic β oxidation [18, 19]. HypothyroidismReduced glucose absorption from gastrointestinal tract accompanied by prolonged peripheral glucose accumulation, gluconeogenesis, diminished hepatic glucose output and reduced disposal of glucose are hallmarks of hypothyroidism [20]. In overt or subclinical hypothyroidism, insulin resistance leads to glucose-stimulated insulin secretion [2]. In subclinical hypothyroidism, diminished rate of insulin stimulated glucose transport rate caused by perturbed expression of glucose transporter type 2 gene (GLUT 2) translocation may lead to insulin resistance. Moreover, due to reduced renal clearance of insulin in hypothyroid conditions, physiological requirements of insulin were diminished.
Anorectic conditions in hypothyroidism may also contribute to reduced insulin in this state. An enhanced dose of insulin is required to ameliorate hypothyroidism, but the therapy warrants caution for adrenal or pituitary failure [21]. Further, symptoms also include increased insulin degradation [23], increased glucagon secretion [24], increased hepatic glucose production [24], enhanced catecholamines, and insulin resistance [25].
These factors have been investigated to be an integral part of hyperthyroidism as well [26]. Hence, an intersection of pathological basis occurs which gives us cue to an array of physiological aberrations which are common in hyperthyroidism and T2DM. Among the above-mentioned symptomatology, insulin resistance has been the most important facet connecting thyroid dysfunction and T2DM. Insulin resistance is a condition which occurs in both hypothyroidism and hyperthyroidism [27].Insulin resistance in the muscles and liver is a characteristic feature of T2DM. Hepatic insulin resistance is characterized by glucose overproduction inspite of fasting hyperinsulinemia, and enhanced rate of hepatic glucose output was the pivotal modulator of increased fasting plasma glucose (FPG) concentration in T2DM subjects [24].
In insulin resistance in the postabsorptive state, muscle glucose is upregulated but the efficiency of uptake is reduced. In the wake of such conditions, reduced glucose uptake into the muscles and enhanced hepatic glucose output lead to worsening of glucose metabolism. The term harmonious quartet is used to address the core pathology of insulin resistance [24]. Deregulated glucose disposal and metabolism in adipocytes, muscles, and liver, along with impaired insulin secretion by the pancreatic beta cells, constitute the four major organ system abnormalities which play a definitive role in the pathogenesis of T2DM.

It is worth considering that insulin resistance has been a proven condition in hyperthyroidism as well as hypothyroidism.
Insulin resistance also leads to impaired lipid metabolism according to recent findings [32].
The higher serum TSH usually corresponds to lower thyroid hormones via negative feedback mechanism. As TSH increased, thyroid hormones decreased and insulin antagonistic effects are weakened. Association of Insulin Resistance in Hyperthyroidism and Subclinical HyperthyroidismHyperthyroidism has been associated with insulin resistance which has been linked with elevated glucose turnover, increased intestinal glucose absorption, elevated hepatic glucose output, increased free fatty acid concentrations, increased fasting and or postprandial insulin an proinsulin levels, and increased peripheral glucose transport accompanied by glucose utilization [27, 34]. T2DM patients with thyroid dysfunction have been proven to be more susceptible to ketosis [35] and ketogenesis [36]. Role of LiverIn hyperthyroidism, endogenous glucose production is elevated and reduces hepatic insulin sensitivity in humans [40] due to glycogenesis and glycogenolysis.
West et al., “Selective modulation of thyroid hormone receptor action,” Journal of Steroid Biochemistry and Molecular Biology, vol. Role of MusclesThere is marked increase in the skeletal glucose utilization in hyperthyroid state [34].
Increased glucose utilization has been reported to be mediated by insulin stimulated glucose oxidation rates [44–46]. Under such conditions, reduced glyco genesis has been reported due to insulin stimulated nonoxidative glucose disposal, which is accompanied by redirection of intracellular glucose towards glycolysis and lactate formation [27]. The transport of lactate from periphery to liver leads to enhanced production of glucose via Cori’s cycle.
Webb, “Thyroid hormone mimetics: potential applications in atherosclerosis, obesity and type 2 diabetes,” Nature Reviews Drug Discovery, vol.
Other studies reported that thyroid hormones are necessary for the mobilization of the tissue lipids especially brown adipose tissues (BATs) which are the fuel for the production of heat [49]. Hypothyroidism and decreased thyroid hormone level are responsible for decreased thermogenesis in BAT. Association of Insulin Resistance in Hypothyroidism and Subclinical HypothyroidismInsulin resistance has been shown to be caused in hypothyroidism in various in vitro and preclinical studies [51–53] where it was found that peripheral muscles became less responsive in hypothyroid conditions.
A possible role of dysregulated metabolism of leptin has been implicated for such pathology [53].
A direct relation between hypothyroidism and insulin resistance has been demonstrated by various authors [15, 54–56]. Subclinical hypothyroidism has been reported to be associated with insulin resistance [55, 57, 58]. However, conflicting findings have also been reported by other workers [59, 60], indicating the need of further investigations in this domain.5. Hall, “The spectrum of thyroid disease in a community: the Whickham survey,” Clinical Endocrinology, vol.
Effect of Thyroid Hormones on the Liver: The Role of GenesVarious genes have been identified which are identified with gluconeogenesis, glycogen metabolism, and insulin signaling.
These include glucose 6 phosphate, protein kinase B (Akt2), β2 adrenergic receptor, inhibitory G protein (Gi), phosphoenolpyruvate kinase (PEPCK) [25], pyruvate carboxylase (PC), GLUT 2 [42, 64], malic enzyme [65], and carbohydrate response element binding protein (ChREBP) [66].
A raised hepatic expression of GLUT 2 in hyperthyroid rats was observed as compared to hypothyroid rats [64].Transcription of various enzymes involved in lipid metabolism has been reported to increase in hyperinsulinemic or insulin-resistant mice [2, 67].
Effect of Thyroid Hormones on the Skeletal MuscleThe various genes which influence the interaction of thyroid hormone and skeletal muscles include GLUT1, GLUT4 [64], β2 adrenergic receptors [69], phosphoglycerate kinase (PGK) [70], PPAR gamma coactivator-1 alpha (PGC-1 alpha) [71], and mitochondrial uncoupling protein [72]. In the skeletal muscles, GLUT 4 has been proven to be mediated by the influence of T3, and it can elevate basal and insulin mediated transport of glucose [64]. Mitochondrial uncoupling protein 3 (UCP 3) is a recently identified gene and has been unveiled to be associated with glucose metabolism and decreased fatty acid oxidation [73].
The role of T2 has also been explored and it has been proven that it is associated with sarcolemmal GLUT-4.
Phosphofructokinase and glycolytic enzymes have been associated with the T2-mediated GLUT 4 activity [74]. A number of genes have been associated with peripheral glucose metabolism [2].Autoimmune causes are reported to be responsible for the genetic dysfunction in the diabetic patient suffering from thyroid related disorders.
However, these findings advocate an immense clinical evidence to support association between T1DM (Type 1 diabetes mellitus) and autoimmune thyroid dysfunction (AITD) [75, 76]. Arrays of genes involved in metabolism of glucose are modulated by active thyroid hormone T3 by binding to the thyroid hormone receptors. Frier, “Frequency of thyroid dysfunction in diabetic patients: value of annual screening,” Diabetic Medicine, vol.
It can be activated via removing an iodine atom from the phenolic ring by the iodothyronine deiodinases type 1 (D1) and type 2 (D2). Type 3 deiodinase (D3) inactivates thyroid hormone by removing an iodine atom from the tyrosyl ring. The deiodinases are expressed in various tissues, and their expression levels vary enormously during development and are regulated by thyroid hormone status.
Type deiodinase (D1) is expressed in liver, while type 2 deiodinase (D2) is expressed in adipose tissue and skeletal muscle. They are involved in regulation of bioavailability of T3 and hence, the response to insulin. It is also associated with a surge in glucose turnover accompanied by an upregulation of insulin-mediated glucose disposal in skeletal muscle and adipose tissue. This phenomenon mediated via positive regulation of insulin sensitive GLUT-4 transcription [78, 79] showed that there were profound genomic effects of T3 on hepatic glucose metabolism. Al-Mughales, “Thyroid dysfunction and thyroid autoimmunity in Saudi type 2 diabetics,” Acta Diabetologica, vol.
TR expressed in the hepatocyte and stimulation of T3-sensitive neurons in the hypothalamus-modulated hepatic glucose production via sympathetic projections to the liver are mediated by circulating glucoregulatory hormones [79]. Recent findings have elucidated polymorphism of deiodinase type 2 (DIO2) gene, Thr92Ala, which suggest homozygosity for this polymorphism which in turn is responsible for enhanced risk of T2DM [80]. A separate meta-analysis indicated that intracellular tri-iodothyronine (T3) is responsible for aberrations in insulin sensitivity [4]. It has also been reported that polymorphism of Thr92Ala leads to a lower activity of type 2 deiodinase which in turn is associated with insulin resistance.
It is a potential modulator of insulin action in skeletal muscle and adipose tissue through the regulation of the GLUT-4 gene transcription [81].Investigations using skeletal muscles in hypothyroid and euthyroid humans have revealed a discernable influence on the downregulated expression of glucose transporter 5 (GLUT 5) but not GLUT 4 [57, 82]. Simultaneous increase in the insulin sensitivity occurs when the levels of thyroid hormone were increased. This phenomenon is governed by intracellular generation of T3 as polymorphisms of DIO2 with reduced T3 generation and also contributes to insulin resistance [80]. In hyperthyroidism, the expression of GLUT 2 is increased as compared to euthyroid state [16]. Zamrazil, “Insulin sensitivity and counter-regulatory hormones in hypothyroidism and during thyroid hormone replacement therapy,” Clinical Chemistry and Laboratory Medicine, vol. In such conditions, perturbations in lipid metabolism further link TH to insulin resistance [16].
Thyroid hormone causes elevation in the plasma fatty acid levels in hyperthyroid conditions but not in hypothyroid conditions. Low intracellular fatty acid levels are associated with hepatic insulin sensitivity via modulation of cellular insulin uptake or lipid oxidation [83]. Fatty acid uptake mediated by TH is a tissue-specific phenomenon and is upregulated in both hypo, and hyperthyroidism [79].Thyrotoxicosis leads to enhanced lipid peroxidation whereas hypothyroidism causes diminished glucose oxidation.
TH instigates upregulation of catecholamine action leading to lipolysis on adipocytes and enhancement of circulating FA. Elevated supply of FA counteracts TH-mediated elevated hepatic long-chain FA oxidative process. Elevated circulating FA levels and availability of gluconeogenic substrates from peripheral reserves reciprocates increased gluconeogenesis in T3-treated animals.
Dimitriadis, “Insulin action in hyperthyroidism: a focus on muscle and adipose tissue,” Endocrine Reviews, vol.
Activation of peripheral substrates explains precipitation of hyperglycemia in thyrotoxicosis [84]. Paradoxically, hyperglycemic effect of thyrotoxicosis can be reversed by increased blood supply to muscles providing a better supply of substrate [16].

Relation of Antidiabetic Therapy (Metformin) and Risk of Thyroid Related PerturbationsCappelli et al. A pilot study on diabetic hypothyroid patient revealed baseline reduction of TSH level after 6 months; similarly a large cohort study on diabetic patients showed significant fall of TSH level in euthyroid patients on L-T4 substitution and subclinical hypothyroid patients who did not receive LT4 treatment, except in euthyroid patients after 1 year on metformin.
Maratou et al., “Thyroid hormones are positively associated with insulin resistance early in the development of type 2 diabetes,” Endocrine, vol. This study concluded that TSH lowering effect of metformin only seen in untreated hypothyroid patient and with L-T4 replacement therapy irrespective of thyroid function test. Metformin has inhibited the cell proliferation and growth-stimulatory effect of insulin on thyroid carcinoma cell lines. Same study showed the stimulation of apoptosis and enhancement in the action of chemotherapeutic agents (doxorubicin and cisplatin) by metformin [89].
Other reports support growth inhibitory effect of metformin in mammalian cell lines mediated by mammalian target of Rapamycin (mTOR) and cyclin D1 [90].7. Therapeutic Role of Thyroid Hormone AnaloguesThyroid hormones have profound influence on various physiological processes ranging from metabolism of lipid, protein, and carbohydrate.
The literature is punctuated with reports claiming antiatherogenic and lipolytic influences of thyroid hormones. Thyroid hormone analogues have paved the way for the development of novel strategies in the treatment of atherosclerosis, diabetes and obesity [91]. The thrust of the research has been in designing TH analogues which are devoid of the cardiac complications [27, 95].
Preclinical investigations have demonstrated that carbohydrate response element-binding protein (ChREBP) is the pivotal transcription factor modulating the stimulation of hepatic lipogenesis mediated by glucose. It has been unequivocally apparent that testing for thyroid dysfunction in T2DM patients is necessary and should be carried out annually [13].
The American Association of Clinical Endocrinologists, Thyroid Disease Clinical Practice Guidelines (2002) recommends thyroid palpation and TSH in diagnosis, especially if goitre or other autoimmune disease presents in association with T2DM. Jaha, “Overview of the diagnosis and management of diabetic ketoacidosis,” American Journal of the Medical Sciences, vol. Regular screening for thyroid abnormalities in all diabetic patients will allow early treatment of subclinical thyroid dysfunction. It has also been proposed that in T2DM patients, a TSH assay should be performed at diagnosis and then repeated at least every 5 years.9.
ConclusionIn internal medicine, it is repeatedly proven that the association between thyroid dysfunction and diabetes mellitus is evident.
Thyroid dysfunction chiefly comprises hypothyroidism and hyperthyroidism although the entity belongs to the same organ but with vast difference in pathophysiology as well as clinical picture. The literature suggests that polyendocrinal multidysfunction leads to stimulation of a cascade of reactions which are actually antihomeostatic in nature. Stockholm, “The influence of the thyroid gland on absorption in the digestive tract,” The American Journal of Physiology, vol. For instance, hypoadrenalism as well as hypopituitarism exhibits strong linkage with hypothyroidism and consequently diabetes mellitus.
Recent findings have evidenced the intricate bond between subclinical hypothyroidism and diabetes mellitus that deceptively contribute to the major complications such as retinopathy and neuropathy. Cardiovascular events and micro- or macro-angiopathies are the counterreflection of resurgence of heavily disturbed lipid metabolism due to thyroid dyscrasias.
It is also evident from the existing literature that insulin resistance bears an indispensable role in connecting T2DM and thyroid dysfunction. Novel molecules have shown the path for the development of suitable thyroid hormone receptor analogues to treat metabolic diseases. Brabant, “The interface between thyroid and diabetes mellitus,” Clinical Endocrinology, vol. Matthews, “Decreased insulin secretion in type 2 diabetes: a problem of cellular mass or function?” Diabetes, vol. Felber, “Study of glucose and lipid metabolism by continuous indirect calorimetry in Graves' disease: effect of an oral glucose load,” Journal of Clinical Endocrinology and Metabolism, vol. DeFronzo, “Pathogenesis of type 2 diabetes mellitus,” Medical Clinics of North America, vol. Arias, “Acute thyroid hormone withdrawal in athyreotic patients results in a state of insulin resistance.,” Thyroid, vol.
Bjorkman, “Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus,” Journal of Clinical Investigation, vol. DeFronzo, “Pathogenesis of type 2 diabetes: metabolic and molecular implications for identifying diabetes genes,” Diabetes Reviews, vol. Wasserman, “Regulation of muscle glucose uptake in vivo,” in Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism, L. Shah, “Association between altered thyroid state and insulin resistance,” Journal of Pharmacology and Pharmacotherapeutics, vol. Raptis, “Thyroid hormone excess and glucose intolerance,” Experimental and Clinical Endocrinology and Diabetes, vol.
Beylot, “Regulation of in vivo ketogenesis: role of free fatty acids and control by epinephrine, thyroid hormones, insulin and glucagon,” Diabetes and Metabolism, vol. Brenta, “The association of insulin resistance with subclinical thyrotoxicosis,” Thyroid, vol. Dimitriadis, “Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease,” Journal of Lipids, vol. Reusch, “Diabetes and cardiovascular disease: changing the focus from glycemic control to improving long-term survival,” The American Journal of Cardiology, vol. Pagano, “Insulin resistance in Graves' disease: a quantitative in-vivo evaluation,” European Journal of Clinical Investigation, vol. Endert et al., “Thyroid hormone effects on whole-body energy homeostasis and tissue-specific fatty acid uptake in vivo,” Endocrinology, vol.
Haber, “Regulation of GLUT2 glucose transporter expression in liver by thyroid hormone: evidence for hormonal regulation of the hepatic glucose transport system,” Endocrinology, vol. Hayashi et al., “Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers,” Journal of Endocrinology, vol. Baylis, “Evidence that thyroid hormones regulate gluconeogenesis from glycerol in man,” Clinical Endocrinology, vol.
Iazigi, “Peripheral glucose metabolism in human hyperthyroidism,” Journal of Clinical Endocrinology and Metabolism, vol.
Sheu, “Peripheral and hepatic insulin antagonism in hyperthyroidism,” Journal of Clinical Endocrinology and Metabolism, vol. Bartak et al., “Effects of hypo and hyperthyroidism on noradrenergic activity and glycerol concentrations in human subcutaneous abdominal adipose tissue assessed with microdialysis,” Journal of Clinical Endocrinology and Metabolism, vol. Hemon, “Effects of hypothyroidism on the brown adipose tissue of adult rats: comparison with the effects of adaptation to cold,” Journal of Endocrinology, vol.
Oppenheimer, “Stimulation and S14 mRNAand lipogenesis in brown fat by hypothyroidism, cold exposure, and cafeteria feeding: evidence supporting a general role for S14 in lipogenesis and lipogenesis in the maintenance of thermogenesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. Bevan et al., “The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats,” European Journal of Clinical Investigation, vol.
Budohoski, “Sensitivity of the soleus muscle to insulin in resting and exercising rats with experimental hypo- and hyper-thyroidism,” Biochemical Journal, vol. Asensio et al., “Hypothyroidism in rats decreases peripheral glucose utilisation, a defect partially corrected by central leptin infusion,” Diabetologia, vol.
Dejax et al., “Response of glucose disposal to hyperinsulinaemia in human hypothyroidism and hyperthyroidism,” Clinical Science, vol. Kautzky-Willer, “Effects of T4 replacement therapy on glucose metabolism in subjects with subclinical (SH) and overt hypothyroidism (OH),” Clinical Endocrinology, vol. Lambadiari et al., “Insulin action in adipose tissue and muscle in hypothyroidism,” Journal of Clinical Endocrinology and Metabolism, vol.

High fasting glucose levels pregnancy rates
Glucose structure discovery


  1. 31.01.2015 at 11:12:39

    Carbohydrates) and starches (complex mixed-meal tolerance test (MMTT) diabetes guidelines do not contain recommendations for fasting.

    Author: Die_Hard
  2. 31.01.2015 at 22:38:21

    Make sure you're keeping your glucose within the less) when.

    Author: Baki_Ogrusu
  3. 31.01.2015 at 19:54:51

    Doubling your snack or, if possible, reducing your insulin dosage to lessen.

    Author: Suner_Girl
  4. 31.01.2015 at 22:37:50

    Intermediate glycemic control is glycated assess the levels of antidiuretic hormone and.

    Author: sex_qirl