Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
introduction to oral hypoglycemic agents with description about sulphonylurea and glinides along with their MOA, indication, side effects and brand name
Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
introduction to oral hypoglycemic agents with description about sulphonylurea and glinides along with their MOA, indication, side effects and brand name
Sulfonylureas for Diabetes: A deep insightRxVichuZ
This powerpoint presentation solely deals with Sulfonylureas, that come under Insulin secretagogues. Their complete pharmacological profile, with pharmacovigilance parameters, important catchpoints and mnemonics have been explained.
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
Sulfonylureas for Diabetes: A deep insightRxVichuZ
This powerpoint presentation solely deals with Sulfonylureas, that come under Insulin secretagogues. Their complete pharmacological profile, with pharmacovigilance parameters, important catchpoints and mnemonics have been explained.
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
Manish yadav .M Pharm First year
Pharmacology . Under -guidence of
Professor Dr. Govind Singh .
M.D.University Rohtak
Department Pharmaceutical science
Pancreas makes a hormone called insulin. It helps your cells turn glucose, a type of sugar, from the food you eat into energy. Diabetes happens when one or more of the following occurs:
Your pancreas does not make any insulin.
Your pancreas makes very little insulin.
Your body does not respond the way it should to insulin
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1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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2. Overview
The pancreas is both an endocrine gland that produces the peptide hormones
insulin, glucagon and somatostatin and an exocrine gland that produces dig-
estive enzymes .
The peptide hormones are secreted from cells located in
the islets of Langerhans(B-cells secrete insulin,A-cells secrete glucagon,D-
cells secrete somatostatin and PP cells secrete pancreatic polypeptide(the
function of which is unknown) .These hormones play an important role in
regulating the metabolic activities of the body, particularly the concentration
of blood glucose.
3. Overview
DIABETES MELLITUS is a chronic metabolic disorder characterised by a high
blood glucose concentration-hyperglycaemia
Fasting plasma glucose >7.0mmol/l, or plasma glucose>11.1mmol/l
2 hours after a meal.
Caused by:
• Insulin deficiency
• Insulin resistance
There are two main types of diabetes mellitus:
• Type1 diabetes (insulin-dependent diabetes mellitus IDDM)
• Type2 diabetes(none- insulin-dependent diabetes mellitus NIDDM)
4. In type 1 diabetes ,there is an absolute deficiency of insulin resulting from
autoimmune destruction of B-cells ,and may it be triggered by an invasion of
viruses or the action of chemical toxins .Patients are usually young(children or
adolescents).Type1 diabetes require exogenous insulin to avoid the catabolic
state that results from life-threatening ketoacidosis.
Type2 diabetes is accompanied both by insulin resistance(which precedes
overt disease)and by impaired insulin secretion,each of which are important
in pathogenesis .Such patients are often obese and usually present in adult
life. the disease is influenced by genetic factors,aging,obesity and peripheral
insulin resistance rather than by autoimmune processes or viruses.
5. Oral hypoglycaemic agents are given orally in the treatment of patients with
type 2 diabetes mellitus whose condition can’t be controlled by diet alone.
These drugs may also be used with insulin in the management of some
patients, use of an oral antidiabetic drug with insulin may decrease the
insulin dosage in some individuals.
types currently in use:
• Biguanides:metformin
• Slufonylureas:glimepiride,glyburide,tolbutamide,glibenclamide,glipizide
• Meglitinides: nateglinide , repaglinide
• Thiazolidinediones: pioglitazone, rosiglitazone
• Alpha-glucosidase inhibitors: acarbose , miglitol
• SGLT2 inhibitors :canagliflozin, dapagliflozin, empagliflozin
• DDP-4 inhibitors:alogliptin,linagliptin,saxagliptin,sitagliptin
• GLP-1 receptor agonist:exenatide,liraglutide
7. Biguanides
Biguanides are old agents that work by reducing hepatic glucose
output and, to a lesser extent, enhancing insulin sensitivity in hepatic
and peripheral tissues (i.e., antihyperglycaemics, hepatic insulin
sensitizers). Phenformin was taken off the market in the United
States in the 1970s because of its risk of causing lactic acidosis and
the associated mortality (rate of approximately 50%). In contrast,
metformin has proved effective and safe . It has been used in Europe
for over thirty years, whereas in the United States it has been
available since 1995. Metformin should be prescribed to all people
with type 2 diabetes, unless contraindicated.
8. Current recommendations of the American Diabetes Association (ADA) and
European Association for the Study of Diabetes (EASD) include metformin, diet
and exercise as first-line therapy for the treatment of patients with type 2
diabetes, irrespective of the presence of overweight status.
Actions and mechanism:
Biguanides lower blood glucose. Their mechanisms are complex and Inco-
mpeletly understood .They increase glucose uptake and utilisation in skeletal
muscle(thereby reducing insulin resistance) and reduce hepatic glucose pro-
duction (gluconeogenesis).Metformin, as well as ,lowering blood glucose,
additionally ,reduces LDL and VLDL, respectively.
Pharmacokinetic aspects
Metformin has a half –life of about 3 hours and is excreted unchanged in the
urine.
9. Side effects:
The commonest unwanted effects of metformin are dose-related gastrointestinal
Disturbanes (e.g. anorexia,diarrhoea,nausea),which are usually not always
transient. Lactic acidosis is a rare but potentially fatal toxic effect ,and
metformin should not be given to patients with renal or hepatic disease,
hypotoxic plumonary disease, heart failure or shock.Such patients are
predisposed to lactic acidosis because of reduced drug elimination or reduced
tissue oxygenation.It should also be avoided in other situation that predispose
to lactic acidosis and in contraindicated in pregnancy .Long-term use may
interfere with absorption of vitaminB12.
10. Thiazolidinediones
Thiazolidinediones also called glitazones( pioglitazone ,rosiglitazone) are a
class of medicines that may be used for the treatment of type 2 diabetes.
They are a type of oral hypoglycemic (a medicine that lowers blood glucose
levels).
Mechanism of action:
Thiazolidinediones bind to a receptor called the peroxisome proliferator
activated receptor-gamma(PPARs ) in adipocytes (fat cells) and promote
maturation of fat cells and deposition of fat into peripheral tissues. By
reducing circulating fat concentrations, thiazolidinediones improve a person
with type 2 diabetes' sensitivity to insulin.
Thiazolidinediones may be used as monotherapy or in combination with other
oral agents for type 2 diabetes, such as metformin or sulphonylureas.
12. Side effects:
Common side effects associated with TZDs include edema, weight gain,
macular edema and heart failure. Moreover, they may cause hypoglycemia
when combined with other anti diabetic drugs as well as decrease hematocrit
and hemoglobin levels. Increased bone fracture risk is another TZD-related
side effect. Thiazolidinediones tend to increase serum low density lipoprotein
cholesterol levels, with rosiglitazone having a more pronounced effect
compared with pioglitazone. Moreover, rosiglitazone increases low density
lipoprotein particle concentration in contrast to pioglitazone where a
decrease is observed
13. Pharmacokinetics and Interactions:
The thiazolidinediones are rapidly absorbed and reach peak concentrations
within a few hours .Steady-state is usually reached within one week, but
perhaps because of the importance of fat redistribution, the full benefit may
take 4 - 12 weeks to become evident. Rosiglitazone and pioglitazone are
strongly protein bound in the circulation, predominantly to albumin .
No significant drug interactions have been reported with the
thiazolidinediones, but it should be noted that in combination with the
sulfonylureas, hypoglycaemia may occur due to the combination of enhanced
insulin sensitivity (thiazolidinediones) and enhanced insulin secretion
(sulfonylureas). Thiazolidinediones are metabolized by cytochrome P450 2C8
(and by CYP3A4 for pioglitazone), but at conventional doses apparently do
not affect the activity of those enzymes. Caution should still be exercised
when using thiazolidinediones in combination with drugs metabolized by
these enzymes.
14. Sulfonylureas
The sulfonylureas were developed following the chance observation that a
sulfonamide derivative (used to treat typhoid) caused hypoglycaemia.
First generation :Tolbutamide,chlorpropamide acetohexamide, and
tolazamide
Second generation:Glibenclamide,glipizide,glimperide,gliclazide and
glimepiride
Mechanism of Action:
Sulfonylureas acts on B cells stimulating insulin secretion and thus reduce
plasma glucose and may slightly improve insulin resistance in peripheral target
tissues (muscle, fat)
15. Their receptor is a component of the ATP-dependent potassium channel in the
pancreatic β-cells; the binding leads to inhibition of these channels, which
alters the resting potential of the cell, leading to calcium influx and
stimulation of insulin secretion. The net effect is increased responsiveness of
β-cells to both glucose and non-glucose secretagogues, resulting in more
insulin being released at all blood glucose concentrations
16. Sulfonylureas differ mainly in their potency and duration of action. The
second generation have a potency that allows them to be given in much lower
doses than the first generation. Drugs with longer half-lives (particularly
chlorpropamide, glibenclamide and glimepiride) can be given once daily. They
cause greater suppression of overnight hepatic glucose output, thereby
lowering fasting blood glucose concentrations more; these benefits, however,
may be counterbalanced by an increased risk of hypoglycaemia. Sulfonylureas
can be used as monotherapy, or in combination with other oral hypoglycemic
drugs or insulin.
17. All sulfonylureas have been associated with weight gain, unless the diabetic
diet and exercise program are followed, and thus are not suggested as first
choice for obese patients. In the UKPDS Study the increment in weight was of
2.6 Kg for those assigned to chlorpropamide and 1.7 Kg for those assigned to
glibenclamide. They are most likely to be effective in patients whose weight
is normal or slightly increased. The choice of sulfonylurea is primarily
dependent upon cost and availability, because their efficacy against
microvascular and cardiovascular complications is similar . Given the
relatively high incidence of hypoglycemia in patients taking glyburide or
chlorpropamide, shorter acting drugs should be preferred, especially in
elderly patients .
18. Side Effects:
Side effects of sulfonylureas may include:
• Signs of hypoglycaemia, such as sweating, dizziness, confusion, or
nervousness
• Hunger
• Weight gain
• Skin reactions
• Upset stomach
• Dark-colored urine
19. Interactions:
• The medicines that may affect how sulfonylureas work include:
• Azole antifungals, including ketoconazole and fluconazole
• Some antibiotics, such as ciprofloxacin, chloramphenicol, sulfonamide,
clarithromycin, rifampin, and isoniazid
• Cholesterol-lowering drugs, such as gemfibrozil, clofibrate
• Tricyclic antidepressants
• H2 blockers
20. • Gout medications, such as sulfinpyrazone and probenecid
• Some high blood pressure medicines, including ACE inhibitors and bosentan
• Beta-blockers
• Corticosteroids
• Calcium channel blockers
• Oral contraceptives
• Thiazide diuretics
• Thyroid medicines
21. Meglitinides
The meglitinides ( repaglinide and nateglinide), are short-acting glucose-
lowering drugs for therapy of patients with type 2 diabetes alone or in
combination with metformin. They were designed to achieve more physiologic
insulin release and less risk for hypoglycemia. They are structurally different
than sulfonylureas but their mechanism of action closely resembles that of
sulfonylureas (they act by regulating ATP-dependent potassium channels in
pancreatic beta cells), because they stimulate the release of insulin from the
pancreatic beta cells through a
22. different binding site on the “sulfonylurea receptor” . Moreover, meglitinides
have different half-life compared to sulfonylureas. Because of the short onset of
action of the meglitinides (15 to 30 minutes), patients should be instructed to
administer a dose immediately before a meal. The meglitinides can be used as
monotherapy, or in combination with other oral hypoglycemic drugs like
metformin, resulting in superior glycemic control than with either agent used as
monotherapy. Their clinical efficacy is similar to that of the sulfonylureas. Some
potential advantages of this class of agents include a greater decrease in
postprandial glucose and a decreased risk of hypoglycemia.
23. Side effects:
Side effects include weight gain and hypoglycaemia. While the
potential for hypoglycemia is less than for those on sulfonylureas, it is
still a serious potential side effect that can be life-threatening.
Patients on this medication should know the signs and symptoms of
hypoglycemia and appropriate management.
Repaglinide (Prandin) caused an increased incidence in male rats of
benign adenomas (tumors) of the thyroid and liver. No such effect was
seen with another drug of this class, nateglinide (Starlix).
24. Interactions:
some drugs can affect how your body processes meglitinides. This may
cause your blood sugar to become too low or too high.
The drugs that might not mix well with meglitinides include:
Azole antifungals
Certain antibiotics, including rifampin and isoniazid
Some high blood pressure medicines, such as calcium channel
blockers, beta-blockers, and thiazide diuretics
Corticosteroids
Estrogen
Nicotinic acid
26. GLP-1 receptor
agonists
Glucagon-like peptide-1 receptor agonists, also known as GLP-1 receptor
agonists or incretin mimetics, are agonists of the GLP-1 receptor.
Glucagon-like peptide-1 (GLP-1) is a 30 or 31 amino acid long peptide
hormone deriving from the tissue-specific posttranslational processing of
the proglucagon peptide. It is produced and secreted by
intestinal enteroendocrine L-cells and certain neurons within the nucleus of
the solitary tract in the brainstem upon food consumption. The initial product
GLP-1 (1–37) is susceptible to amidation and proteolytic cleavage which gives
rise to the two truncated and equipotent biologically active forms, GLP-1 (7–
36) amide and GLP-1 (7–37). Active GLP-1 composes two α-helices from amino
acid position 13–20 and 24–35 separated by a linker region.
Alongside glucose-dependent insulinotropic peptide (GIP), GLP-1 is
an incretin; thus, it has the ability to decrease blood glucose concentration
by enhancing the secretion of insulin
27.
28. This class of medications is used for the treatment of type 2 diabetes. One of
their advantages over older insulin secretagogues, such
as sulfonylureas or meglitinides, is that they have a lower risk of
causing hypoglycemia. GLP-1 as has a short duration of action, so to overcome
this limitation several modifications either in the drug or the formulations are
being developed.
Examples of Approved medicines:
• exenatide (Byetta, Bydureon), approved in 2005/2012
• liraglutide(Victoza, Saxenda), approved 2010
• lixisenatide(Lyxumia), approved in 2016
• albiglutide (Tanzeum), approved in 2014 by GSK
Under investigation:
taspoglutide, phase III halted Sept 2010[
29. Mechanism of action:
enhance glucose-dependent insulin secretion and exhibit other
antihyperglycaemic actions following their release into the circulation from
the gut. GLP-1 receptor agonist that enhances glucose-dependent insulin
secretion by the pancreatic beta-cell, suppresses inappropriately elevated
glucagon secretion, and slows gastric emptying.
30. Side effects:
The most common adverse reactions, reported in ≥5% of patients treated
with Victoza(liraglutide) and more commonly than in patients treated with
placebo, are: headache, nausea, diarrhea and anti-liraglutide antibody
formation.
Immunogenicity-related events, including urticaria, were more common among
Victoza-treated patients (0.8%) than among comparator-treated patients (0.4%)
in clinical trials.
Interactions:
delays gastric emptying. May impact absorption of concomitantly
administered oral medications.
32. Inhibitors of dipeptidyl peptidase 4 (DPP-4 inhibitors or gliptins) are
a class of oral hypoglycaemics that block the enzyme dipeptidyl
peptidase-4 (DPP-4). They can be used to treat diabetes mellitus type
2.
The first agent of the class – sitagliptin – was approved by the FDA in
2006.
Glucagon increases blood glucose levels, and DPP-4 inhibitors reduce
glucagon and blood glucose levels. The mechanism of DPP-4 inhibitors
is to increase incretin levels (GLP-1 and GIP), which
inhibit glucagon release, which in turn increases insulin secretion,
decreases gastric emptying, and decreases blood glucose levels.
33. Drugs belonging to this class are:
• Sitagliptin (FDA approved 2006, marketed by Merck & Co. as Januvia)
• Vildagliptin (EU approved 2007, marketed in the EU by Novartis as Galvus)
• Saxagliptin (FDA approved in 2009, marketed as Onglyza)
• Linagliptin (FDA approved in 2011, marketed as Tradjenta by Eli Lilly and
Company and Boehringer Ingelheim)
• Gemigliptin (approved in Korea in 2012, marketed by LG Life.
34. Side effect:
• including nasopharyngitis, headache, nausea, heart failure, hypersensitivity
and skin reactions.
• The U.S. Food and Drug Administration (FDA) is warning that the type 2
diabetes medicines like sitagliptin, saxagliptin, linagliptin, and alogliptin may
cause joint pain that can be severe and disabling.
35. Interactions:
Possible pharmacokinetic interferences have been investigated between each of
these compounds and various pharmacological agents, which were selected
because there are other glucose-lowering agents (metformin, glibenclamide
[glyburide], pioglitazone/rosiglitazone) that may be prescribed in combination
with DPP-4 inhibitors, other drugs that are currently used in patients with T2DM
(statins, antihypertensive agents), compounds that are known to interfere with
the cytochrome P450 (CYP) system (ketoconazole, diltiazem, rifampicin or with
P-glycoprotein transport (ciclosporin), or agents with a narrow therapeutic safety
window (warfarin, digoxin). Generally speaking, almost no drug-drug interactions
or only minor drug-drug interactions have been reported between DPP-4
inhibitors and any of these drugs.
36. Alpha Glucosidase
inhibitors
Alpha glucosidase inhibitors (AGIs) are a unique class of anti-diabetic drugs.
Derived from bacteria, these oral drugs are enzyme inhibitors which do not
have a pancreato-centred mechanism of action. Working to delay
carbohydrate absorption in the gastrointestinal tract, they control
postprandial hyperglycaemia and provide unquestioned cardiovascular benefit
Examples of alpha-glucosidase inhibitors include:
• Glucobay (Acarbose)
• Glyset (Miglitol)
37. Side effect:
Drug interaction is defined as the modification of effects of one drug by the co
administered drug(s), herb(s), supplements, food, tobacco smoke or alcohol.5
Whereas, the Adverse Drug Interaction is defined as the drug interaction
resulting in elevated risk of adverse effects or decreased therapeutic efficacy.6
As the α-glucosidase inhibitors delay the absorption of carbohydrates, they may
interfere the absorption of certain drugs by altering gastric motility:
• Digoxin:
It has been postulated that absorption of digoxin is interfered by the
coadministration of Acarbose through increased gastrointestinal motility.10 The
interaction between Digoxin and Acarbose may not be clinically significant at
38. • Warfarin:
that Acarbose may increase the absorption of Warfarin.
• Metformin:
The bioavailability of Metformin found to be decreased by the coadministration
of Acarbose.
• Thiazolidinediones:
A study demonstrated that the pharmacokinetics of rosiglitazone altered slightly
and insignificantly by the coadministration of Acarbose.
• Metronidazole :
is an antimicrobial agent and its absorption found decreased in patients with
diabetes taking Acarbose due to increased motility and adherence of Acarbose on
to Metronidazol.
39. SGLT-2 Inhibitors
SGLT2 inhibitors, also called gliflozins, are a class of medications that
inhibit reabsorption of glucose in the kidney and therefore lower blood
glucose They act by inhibiting sodium-glucose transport protein 2 (SGLT2).
SGLT2 inhibitors are used in the treatment of type II diabetes mellitus. Apart
from blood sugar control, gliflozins have been shown to provide significant
cardiovascular benefit in T2DM patients. Several medications of this class
have been approved or are currently under development .In studies
on canagliflozin, a member of this class, the medication was found to
enhance blood sugar control as well as reduce body weight and systolic and
diastolic blood pressure.
40.
41. Side effects:
clinical trials mycotic infections, urinary tract infections and osmotic
diuresis were higher in patients treated with gliflozins.
In May 2015 FDA issued a warning that gliflozins can increase risk of diabetic
ketoacidosis (DKA). By reducing glucose blood circulation, gliflozins cause less
stimulation of endogenous insulin secretion or lower dose of exogenous insulin
that results in diabetic ketoacidosis (DKA). They can also contribute
euglycemic DKA (euDKA) because of the renal tubular absorption of ketone
bodies.
42. Interactions:
Interactions are important for SGLT2 inhibitors because most T2DM
patients are taking many other medications
Gliflozins can increase the diuretic effecof thiazides, loop diuretics and
related diuretics and therefore increase the risk of dehydration
and hypotension. It is important to adjust the dose of antidiabetics if the
treatment is combination therapy to avoid hypoglycemia. For example
interactions with sulfonylureas have led to severe hypoglycemia presumably due
to cytochrome P450.
A study has shown that it is safe to consume dapagliflozin along
with pioglitazone, metformin, glimepiride, or sitagliptin and dose adjustment
is unnecessary for either medication. It is unlikely that food intake has
clinical meaningful impact on the efficacy of dapagliflozin, therefore it can
be administered without regard to meals.